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A HANDBOOK OF 

PATHOLOGICAL ANATOMY 

AND 

HISTOLOGY 

With, an Introductory Section on 

POST-MORTEM EXAMINATIONS AND THE METHODS OF 
PRESERVING AND EXAMINING DISEASED TISSUES 



FRANCIS DELAFIELD, M.D., LL.D. 

Professor of the Practice of Medicine. College of Physicians and Surgeons, 
Columbia College, New York 

T. MITCHELL PRUDDEX, M.D. 

Professor of Pathology and Director of the Laboratories of Histology, Pathology, 

and Bacteriology, College of Physicians and Surgeons, Columbia 

College, New York 



Jfiftb Edition 



ILLUSTRATED BY THREE HUNDRED AND SIXTY-FIVE WOOD 
ENGRAVINGS PRINTED IN BLACK AND COLORS 



NEW YORK 



,8*' 



WILLIAM WOOD AND COMPANY 

1896 






. Copyright by 
WILLIAM WOOD & COMPANY 



PRESS OF 

THE PUBLISHERS' PRINTING COMPANY 

132-136 W. FOURTEENTH ST. 

NEW YORK. 



PREFACE TO THE FIFTH EDITION. 



The aims followed in the preparation of this the fifth edition of 
this work are identical with those which were kept in view in 
former editions. It has been the intention of the authors to give 
to students and practitioners of medicine, first, the knowledge neces- 
sary for the making of autopsies, the preservation of tissues and 
their preparation for microscopic study, and to outline the methods 
of study of pathogenic micro-organisms; second, to describe con- 
cisely, with such illustrations as seem necessary, the lesions of the 
acute infectious diseases and, so far as they are known, the micro- 
organisms concerned in their causation, the various phases of de- 
generation and inflammation, the character of tumors, the special 
lesions of different parts of the body, of the general diseases, of 
poisoning, and of violent deaths. All of the sections of the book 
have been revised, and some of them largely rewritten in the light 
of recent contributions to science. Many new cuts have been added. 
The section on the blood has been rewritten for us by Dr. James 
Ewing. 

FRANCIS DELAFIELD, 
T. MITCHELL PRUDDEK 



CONTENTS. 



PART FIRST. 

THE METHOD OF MAKING POST-MORTEM EXAMINATIONS AND OF 
PRESERVING AND EXAMINING PATHOLOGICAL TISSUES. 

The object in making post-mortem examinations. — Causes of death, 3. — Ex- 
ternal Inspection, 4. — Cadaveric lividity, 5.— Putrefactive changes, 5. — 
Cooling of the body, 6. — Rigor mortis, 7. — Contusions, 7. — Wounds, 8. — 
Fractures, scars, and tattoo marks, 9. — Internal Examination, 9. — The Head. 
Removal of calvarium, 10. — The dura mater, the pia mater, the brain, 
11. — Methods of opening the brain, 11-18. —Base of the cranium, 18. 
— Tlie Spinal Cord, 19. Preservation of cord and membranes, 21. — The 
Thorax and Abdomen, 22. General inspection of abdominal cavity, 23. — 
The heart, 25. — The pleural cavities, the lungs, 28-29. — Pharynx, larynx, 
and oesophagus, 29. — The Abdomen, 30. Kidneys, 31. — Suprarenal capsules, 
32. — The spleen, 33. — Intestines, 34. — Stomach and duodenum, 35. — Liver, 
36. — Pancreas, 37. — Genito- Urinary Organs. Male organs, 38. — Female or- 
gans, 39. 

Autopsies in Medico -Legal Cases and of Suspected Poisoning, 41. 

Examination of the Bodies of New-Born Children. General Inspection, 42. 
—Internal Examination, 46. 

General Methods of Preserving Tissues and Preparing Them for Study, 50. 
— Fresh tissues, 50. — Decalcifying, 51. — Hardening and preservation, 52. — 
Mutter's fluid, 53. — Formalin, osmicacid, Fleming's osmic-acid mixture, 54. 
— Corrosive sublimate, Long's solution, 55. — Embedding and section cutting, 
56. — Staining, 60. — Preservation of museum specimens, 63. 



PART SECOND. 

CHANGES IN THE CIRCULATION OF THE BLOOD.— CHANGES IN THE 
COMPOSITION AND STRUCTURE OF THE BLOOD.— HYPERTROPHY, 
HYPERPLASIA, REGENERATION, DEGENERATION, ETC.— INFLAM- 
MATION. — ANIMAL AND VEGETABLE PARASITES.— INFECTIOUS 
DISEASES. —TUMORS. 

Changes in the Circulation of the Blood. Hyperaemia and anaemia, 69. — 
Haemorrhage and transudation, 69-71. — Thrombosis and embolism, 72-75. 

Changes in the Composition and Structure of the Blood. Coagulability of 
the blood, 76. — Anhydraemia, hydraemia, haemoglobinaemia, anaemia, 76-77. 
Changes in the Red Blood Cells, 77 .—Changes in the White Blood Cells, 82-86. 



VI CONTENTS. 

Melansemia, 86.— Method of examination of the blood, 86-89.— Foreign Bod- 
ies in the Blood, 89. 

Hypertrophy, Hyperplasia, Regeneration, Metaplasia. Hypertrophy and 
hyperplasia, 91. — Regeneration, 91. Direct cell division. — Indirect cell di- 
vision, 92. — Metaplasia, 95. 

Degenerative Changes in the Tissues. Necrosis, coagulation necrosis, 96.— 
Cheesy degeneration, 97. — Parenchymatous degeneration, 98. — Fatty degen 
eration and fatty infiltration, 98. — Amyloid degeneration, 100. — Glycogen 
degeneration, Mucous degeneration, 102. — Colloid degeneration, 103. — 
Hyalin degeneration, 104. — Calcareous degeneration, 105. — Pigmentation, 
106. 

Inflammation, 107. — Degeneration and necrosis, 107. — Congestion, transuda- 
tion, and emigration, 108. — Production of new cells and tissues, 109.— 
Phases of inflammation, 110. — Exudative inflammation, 110. — Productive 
inflammation, 117. — Necrotic inflammation, 119. — Reparative Production of 
New Tissue. — Healing of wounds, 120.— Healing of fractures, 125. 

Parasites. Animal Parasites. Protozoa, 127.— Worms, 130.— Arthropods, 141.— 
Methods of study and preparation of animal parasites, 142. 

Vegetable Parasites. Bacteria, 143.— Morphology and physiology of bacteria, 
144-153. — Classification of bacteria, 153.— Methods of studying bacteria. 
154. — Cultivation of bacteria, 158. — Bacterial examinations of post-mortem 
specimens, 167. — Yeasts and Moulds, 168. — The Relation of Bacteria to Dis- 
ease, 171.— Infection and Immunity, 177. 

The Infectious Diseases, 183. —Infectious diseases induced by the pyo- 
genic bacteria. 188.— Erysipelas, 194.— Pyemia and septicemia, 196 — 
Acute cerebro-spinal meningitis, 199. — Acute lobar pneumonia and the 
infectious diseases induced by the diplococcus pneumoniae, 201. — in- 
fectious pseudo- membranous inflammation of mucous membranes, 204. — 
Gonorrhoea, and other inflammatory lesions induced by the micro- 
coccus GONORRHOEAE, 206.— ANTHRAX, 209. — TUBERCULOSIS, 213-216.— 

Lupus, 227.— Leprosy, 229.— Syphilis, 231.— Glanders, 235.— Rhinoscle- 
roma, 238.— Bubonic plague, 239.— Typhoid fever, 240.— Diphtheria. 
250.— Tetanus, 255.— Influenza, 257.— Bacteria which may be occasional 
inciters of infectious disease in man, 259.— actinomycosis, 262.— asiatic 
cholera, 265.— Relapsing fever, 269. —Variola, 271.— Scarlet fever, 
273.— Measles, 274.— Typhus fever, 275.— Hydrophobia, 276 —Yellow 
fever, 279.— The Malarial Fevers, 280.— Pharyngo- mycosis, 284.— In- 
fectious DISEASES OF ANIMALS, 285. 

Tumors. Section I. General characters, 286. — Cause of tumors, 290. — Classi- 
fication of tumors, 293. — Cysts, 296. — Various lesions sometimes described 
as tumors, 297. — Nomenclature of complex tumors, 297.— Preservation of 
tumors, 298. Section II. Special forms of tumors, 299-343. 



PART THIRD. 

MORBID ANATOMY OF THE ORGANS. 

The Nervous System. The membranes of the brain.— The Dur a Mater, 347. 
Haemorrhages, 347.— Thrombosis.— Inflammation, 348.— Tumors, 351.— The 
Pia Mater, 352. CEdema, hyperaemia, and haemorrhage, 353.— Tuberculous 



CONTENTS. Vll 

meningitis, 359.— Syphilitic meningitis, 362. — Tumors, 362. — The Ventricles 
of the Brain, 365. — Acute and chronic ependymitis, 365. — Congenital hydro- 
cephalus, 367. — Secondary hydrocephalus and primary hydrocephalus in 
adults, 368. — Tumors, 368. — Pineal Gland and Pituitary Body, 369. 

The Brain. Thrombosis and embolism, 370. — Hyperemia, anaemia, and oedema, 
373. — Haemorrhage, 374. — Changes in ganglion cells in toxaemia, 376. — Sec- 
ondary degenerations, 377. — Hypertrophy and atrophy, 378. — Wounds, 379. 
Holes or cysts in the brain, 380. — Inflammation of the brain, abscesses, 380. 
— Chronic interstitial encephalitis (sclerosis), 382. — Encephalitis in new- 
born, 383. — Syphilitic and tuberculous encephalitis, 384. — Lesions of brain 
in chronic paresis of insane, 385. — Pigmentation, tumors, 386. — Malforma- 
tions, 387. 

Spinal Cord. Dura Mater Spinalis. Haemorrhages, inflammations, 389. — Pa- 
rasites, 390. — Pia Mater Spinalis. Haemorrhages, inflammations, 390. — Tu- 
mors and parasites, 391. — The Cord. Haemorrhage, 391. Haematomyeliaand 
haematomyelopore, 391. — Injuries, secondary degenerations, 393. — Progres- 
sive spinal muscle atrophy, bulbar paralysis, amyotrophic lateral sclerosis, 
396-397. — Poliomyelitis anterior, 399. — Chronic myelitis, multiple sclerosis, 
400. — Posterior spinal sclerosis, 402. — Solitary tubercles, gummata, cysts, 
and tumors, 403. — Syringomyelia, 404. — Malformations, 404. 

The Peripheral Nerves. Changes after division, acute and chronic neuritis, 
408. — Tumors, 409. — Acromegalia, scleroderma, 410. — Preparation of nerve 
tissue for microscopical study, 410. 

The Respiratory System. Larynx and Trachea. Malformations, inflamma- 
tion, 413. — CEdema glottidis, tumors, 416. 

The Pleura. Hydrothorax, haemorrhage, inflammation, 417. — Pleurisy with 
production of fibrin, pleurisy with production of fibrin and serum, 418. — 
Pleurisy with production of fibrin, serum, and pus(empyaema), 421. — Chronic 
pleurisy, 423. — Tuberculous pleurisy, 424. — Tumors, 425. 

Tlie Bronchi. Inflammations, 426. — Bronchiectasia, 429. — Tumors, 431. 

The Lungs. Malformations, injuries, congestion, and oedema, 432. — Haemor- 
rhage, 433. — Emphysema, 434. — Atelectasis, 436. — Gangrene, 437. — Inflam- 
mation, classification, acute lobar pneumonia, 438. — Broncho-pneumonia, 
443. — Secondary and complicating pneumonia, 448. — Pneumonia of heart 
disease, 449. — Interstitial pneumonia, 451. — Tuberculous pneumonia, 452. 
— Acute miliary tuberculosis, 453. — Subacute miliary tuberculosis, 456. — 
Chronic miliary tuberculosis, 457. — Acute pulmonary phthisis, 459. — Ex- 
perimental phthisis, 460. — Chronic phthisis, 469. — Syphilitic pneumonia, 
475.— Tumors, 476.— Parasites, 477. 

The Mediastinum, 477. Inflammation, 481. — Tumors, 478. 

The Vascular System. — Pericardium. Injuries, dropsy, haemorrhage, pneumo- 
natosis, 480. — Inflammation, tumors, 483. 

The Heart. Malformations, 483. — Abnormal size and positions of heart, 485. — 
Wounds and ruptures, 486. — Atrophy, hypertrophy, 487. — Dilatation, 489. — 
Degeneration, 490. — Fatty infiltration, atrophy of pericardial fat, 492. — 
Myomalacia, fragmentation of endocardium, 493. — Inflammation, simple 
acute endocarditis, mycotic endocarditis, 494. — Chronic endocarditis. 496. — 
Chronic ulcerative and tuberculous endocarditis, myocarditis, 498. — Changes 
in heart valves, aneurism of the heart, 500. — Thrombosis of the heart, 501. 
— Tumors and parasites, 502. 



Vlll CONTENTS. 

The Blood Vessels. Atrophy and hypertrophy, 502.— Degeneration, 503.— The 
Arteries. Inflammation, acute arteritis, 503. — Chronic arteries, 504. — Dila- 
tation and aneurism, 509. — Aneurism of the different arteries, 512. — Stenosis, 
513. — Ruptures and wounds, 514. — Tumors, 516. — The Veins. Dilatation, 517. 
— Wounds and ruptures, inflammation, 518. — Tumors and parasites, 520. — 
The Capillaries, 520. — The Lymph Vessels, 520. Inflammation, 521. — Lym- 
phangiectasia, tumors, 522. — The Lymph Nodes, 522. Inflammation, 523. — 
Pigmentation, 526. — Inflammation with cheesy degeneration, 527. — Tuber- 
culous inflammation, 528. — Syphilitic inflammation, 529. — Degenerations, 
530. — Hyperplasia, 531. — Tumors and parasites, 532. 

The Alimentary Canal. The Mouth. Malformations, 533.— Hypertrophy of 
cheeks and lips, inflammation, stomatitis, stomatitis ulcerosa, 533. — Syph- 
ilitic and tuberculous stomatitis, gangrene, 534. — Tumors, 535. — The Tongue. 
Malformations, hypertrophy, 536. — Inflammation, tumors, 537. — The Phar- 
ynx and CEsophagus. Malformations, 538. — Inflammation, 540. — Ulcera- 
tion, 541. — Dilatation of oesophagus, 541. — Stenosis, 542. — Tumors, 543. 

The Stomach. Malformations, post-mortem changes, injuries, haemorrhage, 546. 
— Inflammation, 547. — Ulcers, 550. — Dilatation, 553. — Tumors, 554. — Degen- 
erations. The Intestines. Malformations, 557. — Incarceration, 558. — Intus- 
susception, 559. — Transposition, wounds, and ruptures, 560. — Tlie Small In- 
testine. Inflammation, lesions of solitary and agminated nodules, 561. — 
Emboli, 562. — Large Intestine. Inflammations, 563. — Tumors, 575. — Con- 
cretions, parasites, 577. 

The Peritoneum. Malformations, 578.— Inflammation, 579. — Tumors, 587. — 
Parasites, 589. 

The Liver. Malformations, acquired changes in size and position, 590. — Anae- 
mia and hyperaemia, 591. — Wounds, rupture, and haemorrhage, lesions of 
hepatic artery, lesions of portal vein, 593. — Lesions of hepatic veins, atro- 
phy of liver, degenerations, 599. — Pigmentation, 599. — Acute yellow atro- 
phy, 600. — Inflammation, acute hepatitis (abscess), 601. — Chronic intersti- 
tial hepatitis (cirrhosis), 604. — Syphilitic hepatitis, 605. — Tuberculous 
hepatitis, 609. — Perihepatitis, 611. — Hyperplasia of lymphatic tissue in the 
liver, 611.— Tumors, 612.— Parasites, 641. 

The Biliary Passages and Gall Bladder. Catarrhal inflammation, suppurative 
and croupous inflammation, 617. — Constriction, occlusion, and dilatation, 
618.— Biliary calculi, 619.— Tumors, 614. 

The Spleen. Wounds, rupture, and haemorrhage, 621. — Disturbances of the cir- 
culation, 612.— Inflammation, 624.— Perisplenitis, 628.— Alterations of spleen 
in leukaemia and pseudo- leukaemia, 628. — Degenerations, 629. — Pigmenta- 
tion, tumors, 528.— Parasites, 630.— Malformations and displacements, 631. 

The Pancreas. Haemorrhage and inflammation, 632. — Degenerations, 633. — Fat 
necrosis, 634.— Tumors, 635.— Malformations and displacements, 636. 

The Salivary Glands. Inflammation, 637.— Tumors and parasites, 638. 

The Thyroid Gland. Hyperaemia, inflammation, degenerations, and tumors, 
639.— Parasites, malformations, myxoedema, 641.— Exophthalmic goitre, 
643. 

The Thymus Gland, 643. 

The Suprarenal Bodies. Malformations, haemorrhage, thrombosis, inflamma- 
tion, 644. — Degeneration, tumors, 645. 



CONTENTS. IX 

The Urinary Apparatus. The Kidneys. Malformations and changes in posi- 
tion, 646. — Bright's disease, classification, acute congestion, 647. — Acute 
degeneration, 648. — Acute exudative nephritis, 650. — Acute productive ne- 
phritis, 655. — Chronic congestion, 658. — Chronic degeneration, 659. — Chronic 
productive nephritis, chronic Bright's disease, 660. — Suppurative nephritis, 
671. — Ureteritis, 672. — Pyelo-nephritis, 672. — Tuberculous nephritis, embo- 
lism, and thrombosis, 673. — Hydronephrosis, 674. — The cystic kidneys, 675. 
Perinephritis, 676. — Renal calculi, tumors, 677. — Parasites, 680. 

The Urinary Bladder. Malformations, 680. — Changes in size and position, 681. 
Rupture and perforation, 682. Disturbances of circulation, inflammation, 
683.— Tumors, 685.— Parasites, calculi, 687. 

The Urethra. Congenital malformations, and changes in size and position, 688. 
—Wounds, ruptures, and perforations, 689. — Inflammation, 690. — Tumors, 
691. 

The Organs of Generation. Female. — The Vulva. Malformations, haemor- 
rhage, and hyperaemia, 692. — Inflammation, 693. — Tumors and cysts, 694. 

The Vagina. Malformations, changes in size and position, 695. — Wounds, per- 
forations, inflammations, 696. — Tumors, 697. — Parasites, 698. — The Uterus. 
Malformations, 698. — Changes in size, 699. — Changes in position, 700. — Rup- 
ture, perforation, hypersemia, and haemorrhage, 702. — Inflammation, 704. — 
Puerperal inflammation, 708. — Ulceration, degeneration, tumors, 709. — 
Parasites and cysts, 718. — The Ovaries. Malformations, changes in size and 
position, hypersemia, haemorrhage, 719. — Inflammation, 720. — Tumors, 722. 

The Fallopian Tubes. Malformations, changes in position and size, 730. — 
Haemorrhage, inflammation, 731. — Tumors, extra-uterine pregnancy, 732. 

Tlie Placenta. Haemorrhage, 733. — Inflammation, degenerations, 734. 

The Mamma. Malformations, haemorrhage, inflammation, 735. — Tumors, 738. 

Organs of Generation. Male. Tlie Penis. Malformations, 741.— Inflamma- 
tion, tumors, 743.— The Scrotum, 744. — The Testicles. Malformations, hydro- 
cele, 745. — Haematocele, 746. — Spermatocele, inflammation, 747. — Tumors, 
750. — Tlie Seminal Vesicles, 751. — The Prostate. Hypertrophy, 751. — In- 
flammation, 752. — Parasites, concretions, 753. — Coivper's Glands, 753. — 
Tlie Male Mamma, 753. 

The Bones. Disturbances of circulation, injuries, 754. — Inflammation, perios- 
titis, 755.— Osteitis, 757.— Osteomyelitis, 763.— Necrosis, 765.— Caries, 
rachitis, 766. — Osteomalacia, 769. — Alterations of the bone marrow in leu- 
kaemia and anaemia, 770. — Atrophy, tumors, 771. 

Diseases of the Joints. Inflammation, 775.— Tumors, 778. 

Muscle. Haemorrhage, infarction, wounds and ruptures, inflammation, 780. — 
Degenerations, atrophy, pseudo-hypertrophy, 783.— Tumors, 787.— Para- 
sites, 788. 

PART FOURTH. 

THE LESIONS FOUND IN THE GENERAL DISEASES, IN POISONING, 
AND IN VIOLENT DEATHS. 

Diseases Characterized by Alterations in the Composition of the Blood. 
Chlorosis, 791.— Pernicious Anaemia, 792.— Leukaemia, 794.— Pseudo-Leu- 
kaemia (Hodgkin's Disease), 796. 

Scorbutus, Purpura, 798.— H^matophilia, 799. 



X CONTENTS. 

Addison's Disease, 800. 
Gout, 802. 

Acute Eheumatism, 803. 
Diabetes Mellitus, 804. 
Sunstroke, 806. 
Death from Burning, 807. 
Death from Electricity, 808. 

Death from Suffocation, Asphyxia, 809. —Death from Strangulation, Hang- 
ing, 810. — Death from Drowning, 811. 
Death from Poisoning, 814. 









LIST OF ILLUSTRATIONS. 



Fig. Page 

1. Side view of the human brain, showing its fissures and convolutions, . 12 

2. Method of opening the brain, first incisions, 18 

3. Method of opening the brain, final incisions, 14 

4. View of the base of the brain, with the temporal lobes turned backward 

and outward, 16 

5. Drawing of the brain axis, separated from the brain mantle, . . .16 

6. Brain mantle, seen from below, 17 

7. Outlines of spinal cord sections, ........ 21 

Plate. —Blood cells, opposite 80 

8. Phases of mitosis, or indirect cell division, 92 

9. Cheesy degeneration (coagulation necrosis) in miliary tubercle of lung, 97 

10. Fatty degeneration of heart muscle, 98 

11. Fatty infiltration of liver cells, 99 

12. Amyloid (waxy) degeneration of capillaries of a glomerulus in the 

kidney, 101 

13. Corpora amylacea, . . . . . . . .- . . 102 

14. Mucous degeneration of epithelial cells, . 102 

15. Mucous degeneration of fibrous tissue of mamma, 103 

16. Colloid degeneration of epithelial cells, 104 

17. Hyalin degeneration of capillary blood vessels, ..... 104 

18. Pigmentation of connective-tissue cells of the lungs, .... 105 

19. Emigration of white blood cells in inflamed bladder of frog, . . Ill 

20. Exudative inflammation — pneumonia, 113 

21. Exudative inflammation — appendix, . . . . . . 113 

22. Pus cells from catarrhal inflammation of bronchial mucous membrane, 116 

23. Omentum of dog, showing peritonitis on fourth day, .... 116 

24. Developing blood vessels in new-formed tissue, ..... 121 

25. Granulation tissue from wound of skin, . . . . . . . 122 

26. Fibroblasts from granulation tissue, 122 

27. Cicatricial tissue, 123 

28. Exuberant granulations, 124 

29. New-formed cartilage and osteoid tissue from callus after fracture of 

the femur, 125 

30. Amoeba coli, . . . . . . . . . . . .127 

31. Coccidium oviforme, . . 128 

32. Balantidium coli 129 

33. Cercomonas intestinalis, . 129 

34. Trichomonas vaginalis, . 129 

35. Distoma hepaticum, . 130 



Xll LIST OF ILLUSTRATIONS. 

Fig. P AGE 

36. Head of Taenia solium, 131 

37. Head and proglottides of Taenia mediocariellata, 131 

38. Cuticula of echinococcus cyst, 133 

39. Scolices of Taenia echinococcus 133 

40. Hooklets from scolex of Taenia echinococcus, 134 

41. Ascaris lumbricoides, 135 

42. Oxyuris vermicularis, 136 

43. Eggs of nematode worms, . .137 

44. Trichocephalus dispar, . 137 

45. Trichinae encysted in muscle, .139 

46. Filaria sanguinis hominis, . 140 

47. Sarcoptes hominis, 141 

48. Pediculis capitis, 141 

49. Drawing of three typical forms of bacteria, 143 

50. Bacilli showing flagella, . . 144 

51. Growth aggregates of bacteria, 145 

52. Leptothrix buccalis with micrococcus colonies, 145 

53. Sarcina, 146 

54. Bacteria with capsule, 146 

55. Bacilli showing spores, 147 

56. A tube of solid transparent nutrient gelatin, 160 

57. Pure culture of bacteria on nutrient agar, 161 

58. A culture of bacteria on potato, 161 

59. A Petri gelatin plate culture of bacteria, 163 

60. A Petri gelatin plate culture of bacteria, . . . . . . 164 

61. Petri's agar plate culture of bacteria (mouth), 165 

62. Sterilized cotton swab in sterilized tube, 166 

63. Yeast — saccharomyces, 168 

64. Aspergillus glaucus, 169 

65. Achorion Schoenleinii— favus, 169 

66. Bacterial embolus in the blood vessels of the glomerulus of the kidney 

in malignant ulcerative endocarditis, 172 

67. Small focus of necrosis in the liver caused by toxic material of bac- 

terial origin, 173 

68. Colonies of micrococci in a blood vessel of the kidney, causing a small 

abscess, 174 

69. Staphylococcus pyogenes aureus, . 188 

70. Staphylococcus pyogenes aureus in and among the pus cells, from an 

abscess of the kidney, 190 

71. Streptococcus pyogenes, . . 191 

72. Erysipelas of the skin, 194 

73. Streptococci in masses in the blood and lymph vessels of the skin in 

erysipelas, 195 

74. Micrococci in masses in the fibrinous exudation of pyaemic pleurisy, . 197 

75. Diplococcus lanceolatus (pneumococcus) with capsules, . . .201 

76. Pseudo-membranous inflammation of trachea, 204 



77. Infectious croupous inflammation of the trachea, 

78. Micrococcus gonorrhoeae (gonococcus), . 

79. A cover-glass preparation of gronorrhoeal exudate, 

80. Pus cells containing gonococci, 



205 
206 
207 
207 



LIST OF ILLUSTRATIONS. Xlll 

Fig. Page 

81. Anthrax — malignant pustule— of the skin, 209 

82. Bacillus anthracis growing in the blood vessels of the liver of a mouse 

inoculated with pure culture of the bacillus, 210 

83. Bacillus anthracis containing spores, 211 

84. Tubercle bacilli, with pus cells, in sputum, 213 

85. Culture of tubercle bacillus on glycerin agar (bird) , 214 

86. Culture of tubercle bacillus on glycerin agar (man) , 214 

87. A miliary tubercle from a lymph node 216 

88. A miliary tubercle from the pleura, 217 

89. Tuberculous tissue, 218 

90. A nodule of tuberculous inflammation (miliary tubercle) in the lung, . 219 

91. Miliary tubercle in lung of child, showing tubercle bacilli, . . . 221 

92. Inflammatory nodule in the liver of the rabbit, produced by dead 

tubercle bacilli, 222 

93. Lupus of face, 225 

94. The bacilli of leprosy, 229 

95. Small nodule of syphilitic inflammation (miliary gumma) in the liver, 231 

96. New-formed tissue in syphilitic inflammation, 231 

97. Section from a primary syphilitic nodule of the mucous membrane of 

the mouth, 232 

98. Section of a portion of a syphilitic condyloma of the mucous membrane, 233 

99. Bacillus mallei, 236 

100. Cluster of typhoid bacilli in the spleen, 247 

101. Bacillus typhosus, . 248 

102. Diphtheritic inflammation of the tonsil, 251 

103. Bacillus diphtherias, 252 

104. Bacillus tetani, 255 

105. Actinomyces bovis, 262 

106. Actinomyces growing in human bronchus, 263 

107. Spirillum choleree Asiaticaa, 266 

108. Spirochete Obermeieri, 269 

109. A smallpox vesicle of the skin, 271 

110. Section of spinal cord from a case of hydrophobia, .... 276 

111. Hydrophobia, transverse section of small blood vessels in the spinal 

cord, 277 

112. The hsematozoon of malaria, 281 

113. Epithelial cell " inclusions" in tumors, 292 

114. Dense fibroma of abdominal wall, 299 

115. Small papilloma of the skin, 301 

116. Fibroma molle from subcutaneous tissue, . . . . . 301 

117. Myxoma of the larynx, . . .302 

118. Myxoma growing into abdominal cavity, 303 

119. Mucous polyp of the nose, 303 

120. Large spindle-celled sarcoma, 306 

121. Small spindle-celled sarcoma of forearm, . . . . . 306 

122. Small round- celled sarcoma of liver, . . . ... . 307 

123. Large round-celled sarcoma of leg, 307 

124. Melano-sarcoma from submaxillary region, 308 

125. Giant-celled sarcoma of bone, . . . ... . . ' . 309 

126. Angio-sarcoma of liver, 310 



XIV 



LIST OF ILLUSTRATIONS. 



Fig. 

127. Myxo-sarcoma of pharynx, 

128. Adeno-sarcoma of parotid, ... 

129. Endothelioma of upper jaw, 

130. Endothelioma (endothelial sarcoma) of dura mater, 

131. Endothelioma of pleura, 

132. Endothelioma of upper jaw, 

133. Cylindroma (adenoma) of antrum, 

134. Chondroma of subcutaneous connective tissue, 

135. Myxo-chondroma of cervical region, 

136. Glioma of brain, ....... 

137. Neuroglia or " spider" cells from glioma of brain, . 

138. Myoma of uterus, . 

139. Neuroma ganglioniforme, ..... 

140. Fibroma (false neuroma) of lumbar nerve, 

141. Multiple fibromata of pneumogastric nerve, . 

142. Multiple neuromata of the peripheral nerves, 

143. Angioma telangiectoides, 

144. Angioma cavernosum of liver, .... 

145. Congenital lymphangioma from arm of child, 

146. Adenoma of mamma, 

147. Adenoma of stomach, 

148. Cancer cells infiltrating the tissue near a tumor, . 

149. Metastatic carcinoma in lymph vessels of the pleura, 

150. Inflammation in carcinoma, 

151. Epithelioma of the neck, 

152. Metastatic carcinoma (epithelioma) in a lymph node, 

153. Epithelioma of back of hand, . . . . 

154. Epithelioma of axillary lymph node, . . . 

155. Section of a portion of a small epithelioma of the side of the 

power, 

156. Epithelioma of nose, 

157. Carcinoma mammae (schirrhus variety), 

158. Medullary carcinoma of the stomach (carcinoma molle) 

159. Colloid carcinoma of rectum, .... 

160. Carcinoma myxomatodes mammas, 

161. Chronic pachymeningitis interna hemorrhagica, . 

162. Brain sand from pachymeningitis interna, 

163. Acute cellular meningitis, ..... 

164. Acute meningitis, 

165. Acute exudative meningitis, 

166. Fatty degeneration of cells along the blood vessels of the 

exudative meningitis, 

167. A miliary tubercle of the pia mater, 

168. Miliary tubercle of the pia mater of a child, . 

169. A miliary tubercle of the pia mater, 

170. Miliary tubercles of the ependyma of the lateral ventricle, 

171. A miliary tubercle of the ependyma of the lateral ventricle, 

172. Endothelioma of the cerebellum originating in the pia mater, 

173. Endothelioma of the pia mater of the cerebellum, . 

174. Acute ependymitis, • 



nose 



pia mater 



Page 

. 311 

. 312 

. 313 

. 313 

. 314 

. 315 

316 

. 318 

. 318 

. 320 

. 320 

. 321 

. 323 

, 324 

324 

325 

, 326 

327 

327 

330 

331 

333 

335 

335 

337 

337 

338 

, 338 



low 



after 



LIST OF ILLUSTRATIONS. XV 

Fig. Page 

175. Congenital hydrocephalus in child, 367 

176. Degenerated cells, cholesterin crystals, and corpora amylacea from brain 

tissue in embolic softening, 371 

177. Blood vessels from an area of embolic softening of brain, . . . 372 

178. Ganglion cells of the spinal cord, 377 

179. Atrophy of a circumscribed portion of brain convolutions in a child, . 379 

180. Syphilitic obliterating endarteritis of a cerebral artery, . . . 383 

181. Solitary tubercle of cerebellum, . . . . . • . . 384 

182. Haemorrhage in spinal cord, 392 

183. Haematomyelopore, . 392 

184. Descending degeneration, spinal cord, 395 

185. Ascending degeneration, spinal cord, . . 395 

186. Ascending degeneration, spinal cord, 396 

187. Amyotrophic lateral sclerosis, 397 

188. Degenerated tissue, spinal cord, 398 

189. Poliomyelitis anterior, 399 

190. Poliomyelitis anterior, 399 

191. Multiple sclerosis, spinal cord, 401 

192. Posterior spinal sclerosis, . 401 

193. Posterior spinal sclerosis, . 402 

194. Syringomyelia, . ... 404 

195. Hydromyelia, 406 

196. False heterotopia, .406 

197. Multiple neuritis, . 408 

198. Ulcer of larynx, 414 

199. Tuberculous laryngitis, 415 

200. Pleurisy in dog, 420 

201. Tuberculous pleurisy, 425 

202. Catarrhal bronchitis, 427 

203. Croupous bronchitis, . . . . 428 

204. Bronchiectasia, 430 

205. Adenoma of bronchi, 431 

206. Emphysema, 435 

207. Emphysema, 436 

208. Acute lobar pneumonia, 439 

209. Acute lobar pneumonia with organized tissue, . . . . . 440 

210. Acute lobar pneumonia with organized tissue, 441 

211. Acute lobar pneumonia with organized tissue, 442 

212. Broncho-pneumonia, child, ......... 443 

213. Broncho-pneumonia, child, . . 445 

214. Broncho-pneumonia, adult, 446 

215. Broncho-pneumonia, persistent, . . * . . . 447 

216. Broncho-pneumonia, persistent, . 448 

217. Broncho-pneumonia, in diphtheria, 449 

218. Lung of heart disease 450 

219. Interstitial pneumonia, . .451 

220. Miliary tubercle, lung of child, 454 

221. Peribronchitic miliary tubercle, . 455 

222. Aggregation of miliary tubercles, 456 

223. Miliary tubercle, 457 



XVI LIST OF ILLUSTRATIONS. 

Fig. Page 

224. Miliary tubercle, . . . . 458 

225. Miliary tubercle, 459 

226. Experimental pulmonary tuberculosis, rabbit, 460 

227. Experimental pulmonary tuberculosis, rabbit, 460 

228. Experimental pulmonary tuberculosis, rabbit, ..... 462 

229. Tuberculous broncho-pneumonia, 463 

230. Coagulation necrosis and pneumonia, ....... 464 

231. Acute phthisis, . ......... 465 

232. Acute phthisis, 467 

233. Acute phthisis . . .468 

234. Chronic phthisis, . . . . 469 

235. Tuberculous inflammation of lung, . . . . . . . . 470 

236. Chronic phthisis, 470 

237. Chronic phthisis, . .471 

238. Chronic phthisis, . . . .471 

239. Chronic phthisis, . . . . . . 472 

240. Healed phthisis, 473 

241. Tubercle tissue, ■• . . . . . . .474 

242. Syphilitic pneumonia, . 475 

243. Adenoma of lung, 476 

244. Obliteration of pericardial sac, 482 

245. Fatty degeneration of heart, 490 

246. Fatty infiltration of heart, . . 491 

247. Atrophic pericardial fat, . . 492 

248. Vegetation on heart valve, 495 

249. Mycotic endocarditis, ... . . . . . . . 496 

250. Chronic endocarditis, 497 

251. Chronic endocarditis, 498 

252. Chronic interstitial myocarditis, 499 

253. Chronic arteritis, 505 

254. Chronic arteritis, 506 

255. Chronic arteritis, 507 

256. Chronic arteritis, 508 

257. Chronic arteritis, 509 

258. Atheroma of aorta, 510 

259- Atheroma of aorta, 510 

260. Tuberculous arteritis, 511 

261. Tuberculous phlebitis, 519 

262. Inflammation of lymph node, 524 

263. Inflammation of lymph node, 525 

264. Pigmentation of lymph node, 526 

265. Cyst of neck, 539 

266. Cyst of neck, . . . .539 

267. Adenoid polyp of pharynx, 544 

268. Sarcoma of pharynx, 545 

269. Chronic gastritis, 548 

270. Necrosis of mucous membrane of stomach, 553 

271. Fibroma in wall of stomach, • 554 

272. Catarrhal colitis, • • • • 563 

273. Suppurative colitis, 564 



LIST OF ILLUSTRATIONS. xvn 

Fig. Page 

274. Catarrhal colitis, 565 

275. Catarrhal colitis, . ... 565 

276. Croupous colitis, 566 

277. Follicular colitis, . 567 

278. Amoebic colitis, 568 

279. Amoebic colitis, 569 

280. Amoebic colitis . . . . v 570 

281. Amoebic colitis, . . 571 

282. Necrotic colitis, ...... 572 

283. Suppurative appendicitis, 574 

284. Acute cellular peritonitis, 580 

285. Acute exudative peritonitis, 582 

286. Chronic cellular peritonitis 583 

287. Chronic peritonitis, 585 

288. Cystic papilloma of omentum, 588 

289. Chronic congestion of liver, 592 

290. Fatty infiltration of liver cells, 597 

291. Fatty infiltration of liver, 597 

292. Amyloid degeneration of liver, 598 

293. Pigmentation of liver, . 599 

294. Abscess of liver, 603 

295. Chronic interstitial hepatitis, 604 

296. Hypertrophic cirrhosis, . 605 

297. Chronic interstitial hepatitis, 606 

298. Syphilitic hepatitis, . 609 

299. Gumma of liver, 610 

300. Echinococcus multilocularis, 616 

301. Adenoma of gall duct, 619 

302. Congestion of spleen, 622 

303. Chronic indurative splenitis, 626 

304. Chronic interstitial splenitis, 626 

305. Malarial spleen, 627 

306. Amyloid spleen, 630 

307. Fat necrosis in pancreas, . . 634 

308. Colloid struma, 640 

309. Thyroid gland in myxcedema, . 642 

310. Acute degeneration of kidney, 648 

311. Acute exudative nephritis, 650 

312. Acute exudative nephritis, 651 

313. Acute nephritis, 652 

314. Acute nephritis, 653 

315. Acute exudative nephritis, ......... 654 

316. Acute nephritis, 655 

317. Acute productive nephritis, , 656 

318. Subacute productive nephritis, 657 

319. Chronic nephritis with exudation, 663 

320. Chronic nephritis with exudation, , 664 

321. Chronic nephritis with exudation, 665 

322. Chronic nephritis with exudation, 666 

323. Waxy degeneration in kidney, 667 



XY111 LIST OF ILLUSTRATIONS. 

Fig. Page 

324. Chronic nephritis without exudation, 668 

325. Chronic nephritis without exudation, -. . 669 

326. Chronic nephritis without exudation, 670 

327. Cysts of kidney, 675 

328. Adenoma of kidney, 678 

329. Adenoma of kidney, 679 

330. Papilloma of bladder, 686 

331. Vaginal epithelium, 697 

332. Chronic endometritis, 704 

333. Hyperplasia of uterine mucosa, ....... . 705 

334. Chronic endometritis, 706 

335. Uterine phlebitis, . . .708 

336. Adenoma of the uterus, 713 

337. Adenoma of the uterus, 714 

338. Carcinoma of uterus, 715 

339. Epithelioma of uterus, . . . . 716 

340. Fragment of decidua, .......... 718 

341. Chronic oophoritis, 721 

342. Chronic oophoritis, 722 

343. Sarcoma of ovary, 723 

344. Papilloma of peritoneum, .... ..... 724 

345. Cystic adenoma of ovary, 725 

346. Cells from ovarian cyst, . . ._ 726 

347. Cystic adenoma of ovary, . • • • • . . • . 726 

348. Papillary cysts of omentum, 727 

349. Adeno-sarcoma of ovary, 728 

350. Hydro-salpinx, 730 

351. Suppurative mastitis, 736 

352. Chronic mastitis, 737 

353. Intra-canalicular fibroma, 738 

354. Peri-canalicular fibroma, 739 

355. Chronic orchitis, 740 

356. Chronic orchitis, 748 

357. Rarefying osteitis, 758 

358. Condensing osteitis, . . . • • • • . . . 760 

359. Tuberculous osteitis, . . . 761 

360. Rachitic bone, . . 767 

361. Chronic interstitial myositis, • . . 782 

362. Progressive muscle atrophy, 783 

363. Progressive muscle atrophy, 784 

364. Pseudo-hypertrophy of muscle, 785 

365. Hyal in degeneration of muscle, • • 787 



PART I. 



THE METHOD OF MAKING 



POST-MORTEM EXAMINATIONS 



AND OF 



PRESERVING 



AND 



EXAMINING PATHOLOGICAL TISSUES. 



THE METHOD 



OF MAKING 



POST-MORTEM EXAMINATIONS. 



The object in making a post-mortem examination varies in dif- 
ferent cases. It may be to determine whether a person has died 
from violence or poisoning ; to account for a sudden death ; or to 
study the lesions of disease. In any case the examination should 
embrace all the important parts of the body, not merely a suspected 
organ, and it should be recorded at the time it is made. 

In endeavoring to ascertain the cause of death, when the clinical 
history is imperfect or unknown, great care is necessary. Mechani- 
cal causes of death, which destroy life by abolishing the function of 
one of the important viscera, are relatively infrequent. Most of the 
lesions which we find after death indicate rather the ravages of dis- 
ease than the cause of death. We do not know how great a degree 
of meningitis, or of pneumonia, or of endocarditis, or of cirrhosis, or 
of nephritis necessarily causes death. On the contrary, we find that 
one patient recovers with an extent of lesion which is sufficient to 
destroy the life of another. So with accidents ; there is often no 
evident reason why fractures of the skull or of the pelvis should 
destroy life, but yet they usually do. In some of the general dis- 
eases, such as typhoid fever, the visible lesions cannot always be 
called the cause of death; in others, such as typhus fever, there may 
be no evident lesions at all. Sudden deaths of persons who have 
apparently been in good health up to the time of death are often par- 



4: THE METHOD OF MAKING 

ticularly obscure. In many of them we have to acknowledge that 
we can find no sufficient cause for the death. This is of course due 
to our imperfect knowledge, but it is much better in such cases to 
avow our ignorance than to attribute the death to some trifling le- 
sion. The brain and the heart are the organs which are especially 
capable of giving symptoms during life without corresponding lesions 
after death. Very well-marked cardiac or cerebral symptoms ma} r 
continue for days or months, and apparently destroy life, and yet af- 
ter death we find, no corresponding anatomical changes. But it 
should be remembered that recent advances in our knowledge of the 
cell, which an improved technique in hardening and preparation has 
greatly fostered, have already shown that under various abnormal 
conditions the cells, especially of the nervous system, may undergo 
morphological changes of great significance without perceptible alter- 
ation in the gross appearance of the affected part, changes which 
even the microscopical examinations of the past have failed to dis- 
close. So that while there often appears to be a wide discrepancy 
between symptoms and lesions, with the increase of knowledge the 
scope of this discrepancy is steadily narrowing. It is the novice in 
post-mortem examinations who is particularly apt to mistake ordi- 
nary post-mortem appearances for lesions. 

EXTERNAL INSPECTION. 

Before commencing the examination of the internal viscera it is 
always necessary to make some inspection of the external surface of 
the body. The minuteness of this inspection will depend upon the 
character of the case. In the case of an unknown person, or of one 
suspected to have died from unnatural causes, it is necessary to search 
for and record not only all contusions, wounds, etc., their size, situa- 
tion, and condition, but also deformities from disease and any physi- 
cal peculiarities of hair, eyes, teeth, moles, etc., by which the person 
may be identified. In such cases it is well, if possible, to photograph, 
weigh, and measure the body. In cases of doubtful identity it is 
sometimes wise to make a wax or plaster cast of the outside of the 
teeth and jaws. In ordinary examinations we note the general nu- 
tritive condition of the body, and look for evidences of external in- 
jury, for skin diseases, ulcers, oedema, gouty deposits, abscesses, en- 
larged lymphatic glands, etc. The glans penis and prepuce are to 
be carefully searched for syphilitic cicatrices. 

It is usual to find certain changes in the external appearances of 
the body which are due to the cessation of life and the commence- 
ment of decomposition. We speak now of bodies which have not 
been buried, but which have been kept in the ordinary way, lying on 



POST-MORTEM EXAMINATIONS. 5 

the back, and loosely covered with a shroud or dressed with the or- 
dinary clothes. 

Weight. — It is well to weigh the body in all cases. There is of 
course large variation in the weight of individuals within the limits 
of the normal. But these averages may be useful in estimating the 
relative weight of single organs. 

Cadaveric Lividity. — After life becomes extinct, and before the 
blood coagulates, it settles in the veins of the more dependent parts 
of the body, producing, usually within a few hours after death, a 
mottling of the surface with irregular livid patches. These patches 
may coalesce, forming a uniform dusky-red color over the back of 
the trunk, head, and extremities, and sometimes over the ears, face, 
and neck. The same effect is observed on the anterior aspect of the 
body if it has lain on the face. At points of pressure, from folds in 
the clothes or from the weight of the body on the table, the red color 
is absent or less marked. These changes occur before putrefaction 
sets in. This cadaveric lividity or hypostasis should not be mistaken 
for ante-mortem ecchymosis, from which it may usually be readily 
distinguished by its position and extent, by the fact that the surface 
of the skin is not elevated, and by the fact that on incision no blood 
is found free in the interstices of the tissues. Not infrequently the 
subcutaneous tissue in the vicinity of these post-mortem hypostases 
becomes infiltrated with reddish serum. Very soon after death, par- 
ticularly in w T arm weather, the tissues immediately around the sub- 
cutaneous veins of the neck and thorax and in other situations may 
become stained of a bluish-red color from the decomposition and 
escape from the vessels of the coloring matter of the blood. If the 
epidermis has been detached at any point, the skin beneath soon be- 
comes dry and brown. 

Putrefactive Changes. — Usually in from one to three days, de- 
pending upon circumstances, a greenish discoloration of the skin 
appears, at first upon the middle of the abdomen, over which it 
gradually spreads, assuming a deeper hue and often changing to a 
greenish purple or brown. Greenish patches may now appear on 
different parts of the body, earliest upon those overlying the internal 
cavities ; this discoloration is probably produced by the action on the 
haemoglobin of gases developed by decomposition. The eyeballs now 
become flaccid, and if the eyelids are not closed the conjunctiva and 
cornea become brown and dry. The pressure of gases developed by 
decomposition in the internal cavities not infrequently forces a 
greater or less quantity of frothy, reddish fluid or mucus from the 
mouth and nostrils, producing distention of the abdomen, and, if ex- 
cessive, may produce changes of position of the blood in the vessels, 
and even a moderate amount of displacement of the internal organs. 



6 THE METHOD OF MAKING 

After five or six days, under ordinary circumstances, the entire 
surface is discolored green or brown. After this the epidermis be- 
comes loosened from the formation of gases and separation of fluids 
beneath, and the tissues become flaccid. The abdomen and thorax 
may be greatly distended, the features distorted and scarcely recog- 
nizable from swelling, and the hair and nails loosened. Beyond this 
stage of putrefaction the consecutive changes, leading to more or less 
disintegration of the soft tissues, can scarcely be followed with cer- 
tainty. The rapidity with which these changes follow one another 
depends upon a variety of conditions, such as temperature, moist- 
ure, access of air, and the diseases which have preceded or caused 
death. Thus an elevated temperature and the presence of air and 
moisture hasten the advent and progress of putrefactive changes. 
The bodies of infants usually decompose more rapidly than those of 
adults, fat bodies more quickly than lean ones. The infectious dis- 
eases, intemperance, and the puerperal condition promote rapid de- 
composition, as does also death from suffocating gases. Poisoning by 
arsenic, alcohol, antimony, sulphuric acid, strychnin, and chloro- 
form may retard the progress of decomposition. Burial in dry soil 
and submersion in water also retard the progress of decay. 

Cooling of the Body. — The internal temperature of the healthy 
living body is about 37.2° C. (99° Fahr.). But it may be increased 
several degrees in consequence of disease. After death the chemical 
changes upon which the maintenance of this temperature depends 
rapidly diminish, and the body gradually cools to the temperature of 
the surrounding medium. This usually occurs in from about fifteen 
to twenty hours, but the time required depends upon a variety of con- 
ditions. Immediately after death there is, in nearly all cases, a 
slight elevation of internal temperature, owing to the fact that the 
metabolic changes in the tissues still continue for a time, while the 
blood ceases to be cooled by passing through the lungs and periphe- 
ral capillaries. After death from certain diseases — yellow fever, 
cholera, rheumatic fever, and tetanus — a considerable elevation of in- 
ternal temperature has been repeatedly observed. The time occupied 
by the cooling of the body may be prolonged after sudden death 
from accidents, acute diseases, apoplexy, and asphyxia. A number 
of cases are recorded in which the body retained its heat for several 
days without known cause. 

After death from wasting chronic disease, and in some cases after 
severe haemorrhages, the cooling of the body is very rapid, the exter- 
nal temperature being reduced to that of the surrounding air within 
four or five hours. Fat bodies cool less quickly than lean ones, the 
bodies of well-nourished adults less quickly than those of children or 
old persons. The temperature of the surrounding medium, the de- 



POST-MORTEM EXAMINATIONS. ? 

gree of protection of the body from currents of air, will, of course, 
modify the progress of cooling ; and the internal organs naturally 
retain their heat longer than the surface of the body. The rate at 
which cooling occurs is most rapid, as a rule, during the hours imme- 
diately following death, notwithstanding the post-mortem rise which 
may ensue. 

It will thus be seen that if required to pronounce upon the time 
which has elapsed since death in a given case, we can do so only ap- 
proximately. It is necessary to take into account all of the above- 
mentioned conditions which modify the rate of cooling of the body, 
and then we may be able to state only the probabilities of the case. 
It is furthermore unsafe in any case to infer the cause of death from 
the rate of cooling of the body. 

Rigor Mortis. — Death is usually succeeded immediately by a pe- 
riod of complete muscular relaxation. The jaw drops and the limbs 
become flaccid. The muscles may retain for two or three hours, 
however, the capacity of contracting on the application of appropri- 
ate stimuli. On the average within six hours the muscles become 
firm and rigid. This post-mortem rigidity is called rigor mortis. 
On the occurrence of the rigor mortis the muscles become fixed in 
whatever position they may have had at the time of its occurrence. 
It usually begins in the muscles of the eyelids, extends to those of 
the back of the neck and lower jaw, then to the face and neck, and 
thence passing downward affects the muscles of the thorax and 
lower extremities. It usually disappears in the same order. Although 
commencing on the average six hours after death, it may set in al- 
most instantly, or it may be delayed for twenty four hours or more. 
It may pass off very rapidly, in rare cases in from one to three hours ; 
or it may persist for two or three weeks or longer. It may be said 
in general that the average time of its disappearance is within twen- 
ty-four or forty-eight hours after its occurrence, depending on tempe- 
rature, its intensity, the mode of death, the period of its advent, etc. 
Caspar states that in foetuses before term he has never observed rigid- 
ity, and that in young children it is feeble and of short duration. 
Its occurrence and phenomena may be in some cases of the highest 
medico-legal importance; but its careful observation does not, with 
our present knowledge of its significance, appear to essentially fur- 
ther the aims of the practical pathologist. 1 

Contusions. — It is often important to determine whether violence 
has been inflicted upon a body before death. In regard to this point, 
we must remember, first, that blows and falls of sufficient violence 

1 For further details concerning rigor mortis, putrefactive changes, particularly 
the later stages, and the phenomena of cooling of the body, see Tidy, "Legal 
Medicine, " vol. i., pp. 52-120, or other works on medical jurisprudence. 



8 THE METHOD OF MAKING 

to fracture bones and rupture the viscera may leave no marks on tli 
skin, even though the person has survived for several days ; an( 
second, that there are post-mortem appearances which simulate ant< 
mortem bruises. A severe contusion during life may present, i 
first, no mark or only a general redness. After a short time tl: 
injured part becomes swollen and of a red color ; this color may I 
succeeded by a dark blue, and this in turn fade into a greenis 
yellow or yellow ; these later appearances are due to an escape < 
blood from the vessels and to a subsequent decomposition of haem< 
globin. If therefore we cut into such an ecchymosis after death, w 
find extravasated blood or the coloring matter of the blood, in tli 
form of pigment granules, free in the tissues. Post-mortem discoli 
rations, on the other hand, although their external appearance ma 
resemble that of ante-mortem ecchymosis, are not formed by a 
extravasation of blood, but by a circumscribed congestion of tt 
vessels or by an escape of blood-stained serum. If we cut into sue 
discolorations, therefore, we find no blood outside the vessels. 

Blows on the skin of a body which has not been dead for moi 
than about two hours may produce true ecchymoses with extravas; 
tion of blood, such as can be distinguished with great difficulty or n( 
at all from those formed during life. If putrefactive changes \ 
present the difficulty of distinguishing between ante-mortem and pos 
mortem bruises is greatly enhanced. 

Hanging and strangulation are attended with the formation < 
marks on the neck which are fully described in works on f orens 
medicine. These marks must not be confounded with the natur; 
creases of the skin of the neck. Many adults during life ha^ 
creases of the skin of the neck, one or more in number, runnirj 
downward from the ear under the chin or encircling the neck. Af t( 
death these creases may be much more evident than during life, an 
may be rendered more decided by the position of the head and tl 
freezing of the body. They usually persist until the skin putrefies. 

'Wounds. — We should notice the situation, extent, and directic 
of a wound , the condition of its edges and the surrounding tissue 
If it be a deep, penetrating wound its course and extent should I 
ascertained by careful dissection rather than by use of a probe. 

If the edges of a wound be inflamed and suppurating, or con 
mencing to cicatrize, it must have been inflicted some time befoi 
death. In a wound inflicted a short time before death the edges ai 
usually everted ; there may be more or less extravasation of bloc 
into the surrounding tissues, and the vessels contain coagula ; bi 
sometimes none of these changes are observed. The chief characte: 
istics of a wound inflicted after death are, absence of a considerabj 
amount of bleeding, non-retraction of the edges, and the absence ( 



POST-MORTEM EXAMINATIONS. 9 

extravasation of blood into the tissues. But a wound inflicted within 
two hours after death may resemble very closely one inflicted during 
life. In general, unless a wound is old enough for its edges to pre- 
sent inflammatory changes, we must be very careful in asserting its 
ante-mortem or post-mortem character. 

Fractures. — It may be important to determine whether a bone 
was fractured before or after death. This point cannot always be 
decided. Fractures inflicted during life are, as a rule, attended with 
more extravasation of blood and evidences of reaction in the sur- 
rounding tissues ; but fractures produced within a few hours after 
death may resemble these very closely. Usually a greater degree of 
force is necessary to fracture bones in the dead than in the living 
body. 

Scars and Tattoo Marks. — The presence and character of cica- 
trices should be noticed. Scars produced by any considerable loss of 
substance may become very much smaller and less conspicuous, but 
never entirely disappear. Slight and superficial wounds, however, 
produce marks which may not be permanent. The discoloration 
produced by tattooing may, although rarely, disappear during life. 



After completing the external inspection of the body we com- 
mence the internal examination. In order that this examination 
may be made both thoroughly and rapidly, we should follow a regular 
method. The method should be such as will enable us to examine 
the relations of parts to one another, without seriously disturbing 
them, and to remove and inspect the organs in such an order and 
manner as will not interfere with the examination of parts which 
are to follow. In certain cases it may be necessary to depart from 
the regular method ; but, as a rule, the following plan will be found 
most advantageous. 

It is important to remember the difference between the distribu- 
tion of the blood in the body during life and after death. During 
life the blood is in constant motion and is distributed in a regular 
way in the heart, capillaries, arteries, and veins. Inflammations and 
obstructions to the circulation may disturb this natural distribution 
and produce congestion of particular parts of the body. After 
death the blood ceases to circulate ; it leaves the left cavities of the 
heart, the arteries and capillaries, and collects in the veins and the 
right cavities of the heart. According to the character of the dis- 
ease which causes death, coagulation of the blood takes place more 

1 Absolute and relative sizes and weights of various parts and organs of the body, 
and much other valuable statistical data, may be found in Vterordfs "Anatomische, 
Physiologische und Physikalhehe Daten und T ibsllen," Jena, 18S8. 
2 



10 THE METHOD OF MAKING 

or less extensively and at an earlier or later period. The local con- 
gestions which existed during life often disappear after death. On 
the other hand, local congestions are found after death which did 
not exist during life. Thus, after death the scalp often contains a 
large amount of venous blood. The veins of the pia mater and the 
sinuses of the dura mater may be filled with blood. The mucous 
membrane of the larynx and trachea may appear to be deeply con- 
gested. The lungs are congested if the patient has been comatose 
for some hours before death. All the tissues of the back and the 
membranes of the spinal cord are often gorged with venous blood. 
The right auricle and ventricle of the heart may contain fluid or 
clotted blood in considerable quantity. 

THE HEAD. 

The scalp is divided by an incision across the vertex from ear to 
ear. The flaps are dissected forward and backward, taking up the 
temporal muscles with the skin and leaving the pericranium attached 
to the bone. The internal surface of the scalp and the pericranium 
are to be searched for ecchymoses and inflammatory lesions. 

A circular incision is now made through the cranium with a saw. 
The incision should, in front, pass through a point about three and 
one-half inches above the bridge of the nose, behind through the oc- 
cipital protuberance. Care should be taken not to cut through the 
dura mater with the saw. When the roof of the cranium is thus en- 
tirely loosened a stout hook is introduced under the upper edge of the 
calvarium, and this is wrenched off with a jerk. 

Sometimes the. dura mater is so firmly adherent to the calvarium 
that the latter cannot be torn from it without injury to the brain. In 
this case, and also if the dura mater should have been accidentally cut 
through by the saw in making the circular incision, the dura mater 
may be cut through at the level of the cranial incision, and the brain 
removed with the calvarium and separated afterward. Or, which is 
better, in addition to the circular incision, a longitudinal incision is 
made, from front to back, about three-quarters of an inch to one 
side of the median line of the skull, and a segment of bone removed. 
The knife blade may now be inserted from the open side, and the 
dura cut away from the skull-cap along the line of the longitudinal 
sinus, where the adhesions are apt to be most firm. 

We should notice whether or not the calvarium is symmetrical. 
The cranial bones increase in size by a growth of bone at the edges 
of the sutures. If any suture become completely ossified and closed 
prematurely, the bones will be unequally developed. The thickness 
and density of the cranial bones vary considerably within the limits 
of health. There are often deep depressions on the inner surface of 



POST-MORTEM EXAMINATIONS. 11 

the skull along the sagittal suture, caused by the pressure of the 
Pacchionian bodies, and of no pathological significance. We should 
observe the blood content of the bone, determine the existence or 
absence of fractures, inflammatory lesions, exostoses, etc. 

The Dura Mater is now exposed to view. It will be found more 
or less adherent to the calvarium ; a moderate amount of adherence, 
especially in old persons, does not denote disease. Very extensive 
and firm adhesions are usually produced by inflammation. Near the 
median line the Pacchionian bodies often project through the dura 
mater and may produce indentations in the internal surface of the 
calvarium. We must look for clots and for tumors and for inflam- 
matory lesions on the external surface of the dura mater. The 
longitudinal sinus should be laid open and its contents examined. A 
circular incision is then made through the dura mater in a line cor- 
responding to the cranial incision ; the falx is divided between the 
anterior lobes of the brain, and the entire membrane drawn back. 
We should observe the existence of abnormal adhesions of the dura 
mater to the pia mater, bearing in mind that a moderate amount of 
adhesion along the longitudinal fissure is normal. The internal sur- 
face of the dura mater is to ba examined for the products of inflam- 
mation and for tumors. 

The Pia Mater covering the convex surface of the brain is now 
exposed. The degree of congestion, and the existence of serum, pus, 
or blood, beneath, within, or upon it, are now to be ascertained 
before the brain is removed. The pia mater in old persons frequently 
loses its transparency and becomes thick and white ; this change 
is most marked along the longitudinal fissure and large vessels. 
Marked and general thickening of the pia mater is produced by 
chronic inflammation. Along the longitudinal fissure, and some- 
times at a considerable distance from it, we usually find small, ele- 
vated, whitish nodules, which are the Pacchionian bodies and are 
normal in the adult. 

The amount of serum beneath the pia mater varies. A consider- 
able amount, especially in cachectic persons, may exist without brain 
disease. Clear serum raising the pia mater and separating the con- 
volutions of the brain may be simply dropsical or due to chronic 
meningitis. Turbid and purulent serum, beneath and in the pia 
mater, is produced by acute or chronic meningitis. The degree of 
flatness of the surface of the convolutions should be observed before 
removing the brain ; for, when marked, it affords an important indi- 
cation of pressure, from haemorrhage, inflammatory products, inter- 
nal fluid effusions, and tumors. The pia mater should be carefully 
examined for miliary tubercles. 

The Brain. — After examining the convex surface of the brain 



12 



THE METHOD OF MAKING 



the anterior lobes of the cerebrum are to be pulled gently backward, 
the nerves, vessels, and tentorium severed, and the medulla cut 
across as low down as possible. 1 The brain is now removed from the 
cranium by passing the fingers of one hand down, beneath and 
behind the lobes of the cerebellum, and drawing the brain out, sup- 
porting the convexity with the other hand. 

The adult brain in the male weighs on the average about 1,400 
gm. (49^ oz. ) ; that of the female, about 155 gm. (5 oz. ) less. The ave- 
rage proportional weight of the brain to that of the body is about one- 




Fig. 1.— Side View of the Human Brain, showing its Fissures and Convolutions. 






forty-fifth, although in this, as in the absolute weight, there is con- 
siderable variation. 

The exact situation of any lesion which is apparent externally 
should be described by its relation to the lobes, fissures, convolu- 
tions, and sulci. 

The brain is first laid upon its convex surface, and the anterior, 
middle, and posterior cerebral arteries, as well as the basilar and the 
carotids, are to be examined for emboli, thrombi, atheroma, anc 
aneurisms. Evidence of extravasations of blood, tumors, anc 



1 Bailey has devised a knife with a narrow bent blade which can be passed int( 
the upper end of the spinal canal beside the cord and turned so as to cut directlj 
across the latter, in this way avoiding the considerable loss of substance in an im 
portant region of the cord, which the usual oblique cut with a straight knife in 
volves. 



POST-MORTEM EXAMINATIONS. 



13 



inflammatory lesions are now to be looked for. The brain is next 
turned over on to its base. An incision is made through the pia 
mater over the convex surface of the cerebrum. The membrane is 
stripped up, and its adherence to the brain and its thickness noted. 

The more common method of opening the brain is as follows: 
The halves of the cerebrum are to be separated until the superior sur- 




Fig. 2.— Method of Opening the Brain. 
Showing the direction of first incision. 



face of the corpus callosum is exposed (Fig. 2) . A longitudinal incision 
is made through the junction of the corpus callosum and the cere- 
brum, and downward into the ventricle. The incision should be 
made carefully, so as not to cut through the ventricle into the gan- 
glia below. The incision thus made through the roof of the ventricle 
is prolonged backward and forward in the direction of the cornua, so 
as to expose the entire ventricle. A longitudinal incision is then 



14 



THE METHOD OF MAKING 



made outward and backward into the hemisphere, from the oute 
edge of the lateral ventricle, nearly to the pia mater. A second IE 
cision is then made through this cut surface outward, and this i 
repeated until the hemisphere is divided into a number of long 
prism-shaped pieces, held together by the pia mater and a small poi 
tion of the cortex. The brain is now turned around so as to brin 
the other hemisphere under the hand, and the operation is repeate 
on the other side. 

The size, shape, and contents of the ventricles should be noticec 
and the thickness and appearance of the ependyma. 




Fig. 3. — Method op Opening the Brain. 
Showing the unfolded segments of the cerebrum and lines of transverse incision of the bas 
ganglia and directions of the incision of the cerebellum. 

The fornix and the central portion of the corpus callosum are ci 
across by passing the point of the knife through the foramen < 
Munro and cutting upward. They are then drawn backward, 01 
of the posterior cornua of the fornix being severed and laid to 01 
side. The velum interpositum and the choroid plexus are now di 
sected up, the blood contents and the general appearance noted, ar 
the third ventricle examined. Not infrequently small cysts of tl 
choroid are found, which seem to have little or no pathologic 
significance. 

• The fourth ventricle is now opened by a longitudinal incisic 
through the vermiform process. Each hemisphere of the cerebellu: 



POST-MORTEM EXAMINATIONS. 15 

is divided first into two parts by an incision through the upper and 
inner convex border, and then each segment is further divided by 
incisions in the same direction. 

Thin transverse sections are now made through the cerebral 
ganglia, commencing in front (Fig. 3). The ganglia are supported, 
and the sections caused to fall apart as they are cut, by carrying the 
fingers of one hand under the brain, and gently lifting the ganglia 
at points just beneath where the sections are made. It is important 
to observe the exact position of any lesion which may be discovered 
in the cerebral ganglia, their relations to the external and internal 
capsule and to the caudate and lenticular nucleus. 

Finally the segments of the cerebrum and cerebellum are folded 
up together into their original positions, the whole is turned over on 
to the vertex, and thin sections are made through the medulla. 
Small clots in the medulla should not be overlooked. 

In case of the discovery of apoplectic clots, areas of softening, 
etc. , either in the hemispheres or in the basal ganglia, after their 
location and extent are determined they should be carefully searched 
for lesions of the blood vessels, minute aneurisms, areas of degenera- 
tion, and ruptures. For this purpose it may be necessary to allow 'a 
stream of water to run over the affected portion, so as to wash out 
the brain substance and expose the vessels. In some cases the blood 
vessels are best exposed by macerating the brain tissue at the seat of 
the lesion for some hours in water, and then washing out the brain 
substance under the faucet. 

While the above mode of dissecting the brain gives a very com- 
plete view of the seat and extent of lesions in general, where a more 
exact localization of lesions with a microscopical examination is to be 
made the following is a better method of opening the brain : 

After completing the external examination, as detailed above, the 
brain is laid on its vertex, the cerebellar end toward the operator. 
The cerebellum is raised by the fingers of the left hand, and the pia 
cut through along the sides of the corpora quadrigemina, around the 
crura and along the inner margins of the temporal lobes to the middle 
cerebral artery on both sides (Fig. 4) . Then, raising the temporal 
lobes, in turn, by their apices, the pia is cut through along the course 
of the middle cerebral artery into the Sylvian fissure, and along the 
course of its posterior branch to its end. Now drawing the temporal 
lobes one after the other upward and outw r .ard, their junction with 
the base is cut, the knife being held horizontally so as not to injure 
the basal ganglia, until the descending horn is opened. The point 
of the knife being in the descending horn, the incision through the 
brain substance then passes outward and backward well into the 
posterior horn, thus partially severing, at the lateral surface of the 



16 



THE METHOD OF MAKING 



brain, the junction of the occipital and temporal lobes. The ten 
poral lobes are then turned outward and backward (Fig. 4). 

The operculum is now pulled well outward, completely exposir 




Fig. 4.— Schematic Picture of Brain. 
Showing the method of dissection from the base (Meynert's method). E and F, Temporal lot 
turned backward and outward; A B, A C, B D, line of incision to remove basal piece. 

the island of Reil, and a slightly curved transverse incision is mad 
deep enough to pass into the anterior horns of the ventricles, coi 
necting the anterior sulci of the island of Reil (Fig. 4, A, B). 




Fig. 5.— The Brain Axis separated prom the Brain Mantle, as seen from above. 



Now raising the cerebellum and inserting the point of the knii 
into the ventricle, with short incisions from within outward ci 



POST-MORTEM EXAMINATIONS. 



17 



through the internal capsule on either side from back to front (Fig. 
4, C A and D B) care being taken not to injure the basal ganglia. 
Then cut across the crura of the fornix and the septum lucidum, 
leaving the fornix lying on the corpus callosum. 

The square basal piece thus freed — the brain axis — includes the 
island of Reil, the basal ganglia, the crura, pons, medulla, and cere- 
bellum (Fig. 5). 

The remaining portion— the brain mantle — includes the convolu- 
tions, corpus callosum, and fornix (Fig. 6). 

The basal piece may be further examined by a series of transverse 




Fig. 



-The Brain Mantle as seen from below. 



A, Internal capsule B, operculum ; C, posterior border of corpus callosum ; D, descending 
horn : E, cornu Ammonis. 

incisions from one-half to three-quarters of an inch apart, and it may 
be hardened either with or without the cerebellum. The convolu- 
tions may be cut into small pieces by longitudinal and transverse 
incisions, made from within and not reachmg quite to the pia mater, 
which will then serve to hold the pieces together in their proper 
relations to one another. 1 



1 For further details of this method of opening the brain and a consideration of 
its advantages, see Van Gieson, Laboratory Notes, etc. , New York Medical Journal, 



July 20th, 1889. 
3 



18 THE METHOD OF MAKING 

For the methods of hardening and preserving the brain tissues 
see below. 

The Base of the Cranium. — We now return to the skull. Th( 
remaining sinuses of the dura mater should be opened, and this 
membrane then entirely stripped from the bone. The bones at th< 
base of the skull are to be examined for fractures, inflammatory 
lesions, and tumors. In cases of acute purulent meningitis th< 
temporal and frontal bones should be carefully examined, as th< 
inflammatory process is sometimes transmitted from the internal ear 
or mastoid cells, or frontal sinuses. 

The eyes may be removed by breaking the roof of the orbit wit! 
a hammer, removing the fragments of bone, and dissecting awaj 
bone and muscles, so as to expose the optic nerve and posterioi 
segment of the eye. That portion of the globe which is not coverec 
by conjunctiva can now be cut away with scissors and removed witl 
the optic nerve, or, when permissible, the whole eye may be cut out. 

The examination of the internal ear may be made by removing 
its entire bony encasement with the saw and chisel, or by the expo 
sure of special parts by hammer and chisel, and by suitable opening 
of the removed parts with a fine saw. 

Hardening and Preservation of the Tissues for Microscopical Examination. — Foi 
the study of tumors and inflammatory lesions of the bones of the skull and ossifica 
tions of the dura mater and pia mater, the affected portions should be cut into smal 
pieces, decalcified, and subsequently hardened in strong alcohol. In the ordinary 
lesions of the dura mater, the tissues are best hardened and preserved by stretching 
the diseased portions on a flat piece of wood or cork with pins, and hardening then 
in Muller's fluid or alcohol. ! 

The pia mater is so delicate that if it be separated from the brain when quit< 
fresh its tissues are apt to be injured. The portions of the pia mater which are t( 
be preserved should therefore be removed by cutting off slices of the brain substance 
about half an inch thick, with the membrane still attached, and placing the whol( 
in Muller's fluid. After twenty-four hours the pia mater will have become suffi 
ciently hard to permit of its being stripped cff without injury, and it is then spreac 
loosely on a flat cork with pins, the free surface outward, and the cork floated, 
specimen side down, in a dish of alcohol (eighty per cent). The next day strong 
alcohol may be used, and the hardening is complete in three or four days. The pis 
mater should not remain longer than twenty-four hours in Muller's fluid befon 
being stripped off, for after this time it usually becomes so firmly attached to the 
brain substance as to render its removal very difficult. 

When sections are required showing the pia in its relationship to the underly 
ing brain tissue, small blocks of the brain and pia together should be cut out anc 
hardened in Muller's fluid or in alcohol, or in formalin (2 : 100) solution (se( 
page 53). 

When the ependyma is to be studied apart from the associated nerve tissue it maj 
be sliced off with a sufficient quantity of underlying brain substance to prevent it: 



JFor details of the methods of hardening, decalcifying, staining, etc., see the enc 
of Part I. 



POST-MORTEM EXAMINATIONS. 19 

folding, and hardened in Muller's fluid. Special care should be exercised not to 
touch the surface of the ependyma, since the epithelium is easily rubbed off. 

The brain substance, after having been cut into sufficiently small pieces for the 
general examination, should be hardened in Muller's fluid. Large quantities of the 
fluid should be used, four or five times the bulk of the tissue, and the pieces of tissue 
should either be suspended in gauze or kept apart by a little absorbent cotton. The 
fluid should be kept cool, and changed on the second, fifth, and eighth days, and 
again in the third week. 

In general, two or three months are required to secure a good hardening with 
Muller's fluid. When the hardening is complete the brain tissue is rinsed off with 
water and put in. eighty -per-cent alcohol, in which it may be kept, preferably in the 
dark. 

Great care is required in hardening and preserving nerve tissues, and most of the 
ordinarily practised methods give only caricatures and gross distortions of the brain 
structure. 

Too long a soaking in Muller's fluid renders brain tissue very brittle. To get the 
best hardening the single pieces ought not to be larger than 1 c.c. 

Hardening in sublimate solution for many purposes, especially for studies on the 
ganglion cells, gives excellent results. 

Certain lesions, particularly the softenings of the brain, are best studied by teas- 
ing, when fresh, in one-half-per-cent solution of sodium chloride, or in frozen sec- 
tions of the fresh tissue. 

The blood-vessels should be stretched on cork with pins and hardened with 
Muller's fluid and alcohol. The eye and portion of the optic nerve, if removed, 
should be hardened with Muller's fluid. 

Mliller's fluid is especially useful for the preservation and hardening of the nerve 
fibres and neuroglia. The ganglion cells are better preserved in sublimate, formalin, 
or even in alcohol. 

Yan Gieson 1 has called attention to the value of formalin for the hardening of 
the brain and spinal cord. It should be used in from four- to ten-per-cent solution 
for ten days and the hardening completed with " graded " alcohols — that is, alcohol 
used in successive portions of gradually increasing strength. 

In this way the ganglion cells, nerve fibres, and neuroglia are all well preserved, 
and the tissue may be stained by either Weigert's hematoxylin method or Nissl's 
method, although for the latter purpose the hardening is not quite so good as by 
absolute alcohol. 



THE SPINAL CORD. 

The examination of the spinal cord is usually most conveniently 
made after the removal of the brain. 

The body should be placed face downward, with a block under 
the thorax and the head hanging over the edge of the table. An in- 
cision is made through the skin and muscles along the entire length 
of the spine, and the soft parts dissected away on each side so as to 
expose the laminae of the vertebral column. The laminse are then 
divided close within the articular processes with the saw. 

The saw should be so directed in severing the laminse that the in- 

1 Van Gitson, Anatomische Anzeiger, Bd. x., No. 15, 1895. 



20 THE METHOD OF MAKING 

cision shall touch the outer border of the spinal canal, as otherwise 
the laminae and spinous processes are not easily separated. 

Great care should be taken on the one hand not to injure the core 
with saw, and on the other to completely loosen the portions of bom 
to be removed. These, which are the spinous processes and laminae 
are now torn away together with a stout hook, exposing the cord. 

By means of a long, curved chisel, made for this purpose, th< 
bodies of the vertebras may be removed from the front after the tho 
racic and abdominal viscera are taken out, and the cord thus exposec 
and removed. 

But in this anterior method of removing the cord, as well as b^ 
the use of chisel and mallet, bone shears, etc., in the ordinary method 
there is great liability of injuring the delicate tissues of the cord anc 
producing, as Van Gieson has shown, 1 mechanical alterations whic] 
are liable to be mistaken for malformations or the effects of disease. 

"When the body has lain on the back, the membranes of the core 
may be found considerably congested without indicating the pre-ex 
istence of any disease. If the body has lain for some time, especially 
in warm weather, serous fluid may have accumulated within thi 
membranes as a result of post-mortem change. 

The roots of the nerves are now to be cut across, as far away ai 
possible from the cord, and the cord removed in its membranes, car< 
being taken not to press it in any way. It is the safest plan not t( 
grasp the cord itself, but with a forceps to seize the dura mater anc 
thus lift it up at once as it is freed from its attachments. It is nov 
laid on the table, and the dura mater laid open with scissors on th( 
anterior and posterior surfaces over its entire length, and searchec 
for tumors, inflammatory lesions, etc. The finger should be passec 
gently along the cord as it lies on the table, so as to detect anj 
marked softening or sclerosis. The weight of the spinal cord is f roir 
33 to 38 gm. It should now be held lightly over the fingers, anc 
smooth transverse incisions made, with a very sharp knife or razor, 
about half an inch apart through its entire substance between the 
segments, leaving these attached to the pia mater. 

The segments of the spinal cord are those parts from which the 
spinal nerves arise, and it is convenient for the location and descrip- 
tion of lesions to number the segments in correspondence with the 
nerves which arise from them and to indicate on outline diagrams oi 
the cord the exact seat of small lesions. 

The cut surfaces should be carefully examined for abnormal blood 
contents, haemorrhages, inflammatory lesions, softening, scleroses. 

1 Van Gieson, " A Study of the Artefacts of the Nervous System, " New York 
Medical Journal, 1892. 



POST-MORTEM EXAMINATIONS. 



21 



and pigmentations. Important lesion of the cord may be invisible to 
the naked eye, and hence, if disease be suspected, the organ should 
be preserved for microscopical examination. After removal of the 







Fig. 7.— Outlines of Sections of the Spinal, Cord at Different Levels. 

Copies of these outlines may be used for memoranda of the situations of lesion of the spinal 
cord. I, Second cervical; II, fifth cervical; III, eighth cervical; IV, first dorsal; V, eighth dorsal; 
VI, third lumbar; VII, fourth sacral. 

cord fractures and displacements of the vertebrae are easily recog- 
nized. 

Preservation of the Spinal Cord and its Membranes, and of Peripheral Nerves. — 
After the removal of the spinal dura, the entire cord with its nerve roots — the seg- 
ments into which it has been cut for gross examination being left in place — should 
be laid on a wad of absorbent cotton in a large jar of Muller's fluid, the segments 



22 THE METHOD OF MAKING 

being slightly separated from each other by a little absorbent cotton. Van Gieson 
recommends the careful, rolling of the segmented cord into a loose spiral and laying 
this coil on a wad of absorbent cotton in the Miiller's fluid. In this way the cut 
ends of the segments are held apart and accessible to the preservation fluid, and 
harden with little distortion. 

The hardening and preservation of the cord should be done by the same method as 
suggested above for the brain. The same care should be exercised as in the brain 
not to permit the cord to become brittle by remaining too long in the Miiller's fluid. 
If the dura mater of the cord alone is to be preserved, it should be treated in the 
manner suggested for the dura mater cerebralis. The pia mater spinalis is best 
studied in sections through the entire cord, the membranes being left in situ. 

Peripheral nerves may be hardened in Miiller's fluid, care being taken that they 
do not become brittle by too long soaking in it. The hardening is completed and 
the specimen preserved in alcohol, Kitchel has shown that the axis cylinder is well 
preserved in strong formalin solutions (twenty -five per cent) . 

For the hardening of the peripheral nerves osmic acid is very useful, especially 
when changes in the myeline are to be sought after. 

As osmic acid does not readily penetrate the lamellar sheath so as to come in con- 
tact with the nerve fibres, in trunks of any considerable size, the following proce- 
dure as suggested by Van Gieson will be found useful : A piece about one-half inch 
long is cut from the nerve to be examined, and, seizing one end of this segment with 
a forceps, with another forceps the individual nerve fibres, or small clusters of these, 
are pulled out of the lamellar sheath and put at once in one-per-cent aqueous solu- 
tion of osmic acid, in which they remain twenty-four hours, and are then washed 
and transferred to glycerin, to which twenty-five per cent alcohol is added. In this 
mixture they may be preserved. 

THE THORAX AND ABDOMEN. 

To examine these cavities the body is replaced on its back, and 
a single straight incision is made from the top of the sternum to the 
pubes, passing to the left of the umbilicus. For this purpose a large 
knife should be used, held firmly in the whole hand, and the move- 
ment should be mainly from the shoulder. The first incision should 
divide everything down to the sternum and peritoneum. A short 
incision should then be made through the peritoneum, just below the 
ensiform cartilage. Into this opening two fingers of the left hand 
are introduced and separated from one another, and, the parietes 
being raised and the sides of the opening being held apart by the 
fingers, the peritoneum is divided to the pubes, care being taken to 
hold the knife horizontally so as not to cut the intestines. The skin 
and muscles are then dissected off from the thorax on both sides as 
far back as the false ribs. 

This dissection should be made by long sweeps of the knife, which 
should be made to cut with the full blade and not with the point 
only ; and if the skin and muscles be pulled strongly away from the 
chest with the left hand, it may be done very rapidly and with a few 
strokes of the knife. We notice here the amount of subcutaneous 
fat and the condition of the muscles. In order better to expose the 



POST-MORTEM EXAMINATIONS. 23 

abdominal cavity, the rectus abdominis muscles should be divided 
transversely beneath the skin just above the pubes, and the abdomi- 
nal flaps may then be turned freely outward. 

General Inspection of the Abdominal Cavity. — We first notice 
the position and general condition of the viscera. It is best at this 
stage of the examination to note the condition of the vermiform 
appendix, and to look over the peritoneal cavity for serum, inflam- 
matory lesions, evidences of perforation, and for the existence of 
invagination, incarceration, and herniee of the intestines. A small 
quantity of reddish serum is frequently found in the abdominal 
cavity, particularly in warm weather, as the result of commencing 
decomposition. 

It should be remarked here that a variety of striking changes in 
the character and appearance of the internal organs are produced by 
putrefaction — changes which are often mistakenly regarded as evi- 
dences of disease, and much experience is required in judging 
correctly of their significance. These changes are, in general, soft- 
ening and discoloration, both of which may occur as the result of 
disease. It may be said in general that the post-mortem reddening 
or hypostases are most marked in the more dependent parts of the 
organs. Post-mortem softening usually affects entire organs, not 
being limited to a part as is often the case in disease. Gray or 
greenish-brown post-mortem discolorations are apt to appear in those 
organs or parts of organs which lie in contact with the intestinal 
canal. Parts of internal organs, such as the liver, which have been 
the seat of localized congestion during life, may after death take 
on a dark-greenish color. 

The omentum is usually spread over the surface of the small 
intestines, but it may be rolled up and displaced in a variety of ways, 
( r may be adherent at some point to the small intestines or the 
abdominal wall. 

The surface of the small intestines should be smooth and shin- 
ing. They may be greatly distended with gas, and thus so com- 
pletely cover the other abdominal viscera that it becomes necessary to 
let out some of the gas by a small puncture. The transverse colon 
passes across the abdomen through the upper part of the umbilical 
region. It may be lower than the umbilicus or higher up against 
the liver and diaphragm ; it may be distended with gas or con- 
tracted. 

The liver is situated in the right hypochondriac and epigastric 
regions, filling the concavity of the diaphragm. Its upper border 
reaches, in the linea mammillaris, to the fifth intercostal space ; in 
the linea axillaris, to the seventh intercostal space ; close to the ver- 
tebral column, to the tenth intercostal space. At the median line the 



24 THE METHOD OF MAKING 

upper border of the liver corresponds to the lower border of tl 
heart. The left lobe extends about three inches to the left of ti. 
median line. The lower border of the right lobe usually reaches 
the free border of the ribs, while the left lobe is visible for about i 
inch below the ensiform cartilage. In women the liver is usual 
lower than in men. 

The position of the liver is affected by changes in the thorac 
cavity, forcing it downward ; by changes in the abdominal cavit 
forcing it upward ; by constriction of the waist in tight lacin 
forcing it either upward or downward ; by changes in the size of 1 
organ itself. The liver may not only be displaced downward b 
dislocated, so that its convex surface faces the abdominal wall ai 
its posterior edge is turned upward against the diaphragm. 

The stomach is situated in the left hypochondriac and epigasti 
regions, extending also into the right hypochondrium ; it lies in pa 
against the anterior wall of the abdomen, in part beneath the liv 
and diaphragm, and above the transverse colon. Its anterior surfac 
which is directed upward and forward, is in contact above with tl 
diaphragm and the under surface of the liver, and lower down wii 
the abdominal wall opposite to the epigastric region. Its posteri< 
surface is turned downward and backward, and rests on the tran 
verse mesocolon, the pancreas, and the great vessels. To its less< 
curvature or upper border are attached the gastro-phrenic ligamei 
and the gastro-hepatic omentum. To the greater curvature < 
lower border is attached the gastro-colic omentum. Its cardie 
orifice communicates with the oesophagus, its pyloric end with tl 
duodenum. 

When the stomach is distended the greater curvature is elevate 
and carried forward, the anterior surface is turned upward and tl 
posterior surface downward. When distended with food or gas tt 
organ is prominent ; when empty it may hardly be visible belo 1 
the ribs ; when the intestines are dilated it may be entirely covere 
by them. 

Before opening the thorax the hand should be passed up agaim 
the under surface of the diaphragm on either side to determine il 
height. According to Quain, the vault of the diaphragm rises, i 
the dead body, on the right side to the level of the junction of th 
fifth rib and sternum, on the left side as high as the sixth rib. Bot 
the relative and the absolute height of the diaphragm vary under 
variety of pathological conditions. 

If the existence of air or gas in the pleural cavities be suspected 
the abdominal cavity should be filled with water and the diaphragr 
punctured below the level of the fluid. If air be present it wi 
escape in bubbles through the water. 



POST-MORTEM EXAMINATIONS. 25 

THE THORAX. 

We now leave the abdominal viscera and proceed to the exami- 
nation of the thorax. With a costatome or a strong knife the 
costal cartilages are divided close to the ribs, the clavicles are dis- 
articulated from the sternum, and the latter removed, taking care 
not to wound the large veins. We first examine the position of 
the heart and lungs. 

The Heart. — The upper border of the heart is on a level with the 
third costal cartilage ; the lower border extends from 1.3 cm. (i in.) 
below the lower end of the sternum to the fifth left intercostal space. 
The left boundary of the heart is situated to the left of the junction 
of the fifth rib with its costal cartilage, and behind or to the left of a 
vertical line drawn downward from the left nipple. The right 
boundary extends about 2.5 cm. (1 in.) to the right of the right edge 
of the sternum. The portion of the heart uncovered by the lungs is 
of an irregular quadrangular shape. Its lateral diameter is from 
3.8 cm. to 11.1 cm. (1^-4^ inches); its upper boundary varies from 
the level of the second costal cartilage to that of the fifth, but it i& 
usually behind the third or fourth cartilage or fourth space. 

The area of the heart which is found uncovered will, however, 
vary much according to the degree to which the lungs collapse af tei 
opening the chest. Any disease which diminishes the size of tht 
lungs, or pleuritic adhesions which retract or bind them down, may 
increase the area of exposed heart. On the other hand, emphy- 
sema, pneumonia, or any disease which increases the size of, or re- 
tains the air in, the lungs, may diminish the area of exposed heart. 
The exposed area varies also with the size of the heart itself. 

The Pericardium is now opened by a slightly oblique incision ot 
its anterior surface. The existence of serous, fibrinous, or purulent 
exudation, and of adhesions, is to be noticed. A small quantity or 
clear serum exists normally in the pericardial sac, and this serum 
may be blood-stained from beginning decomposition. White thick- 
enings of the pericardium on the surfaces of the heart are often seen; 
they do not indicate important disease. 

Now that the pericardial sac is open, the position of the heart can 
be clearly seen. It lies obliquely in the chest, its long axis at an 
angle of about 60 degrees with that of the thorax. The portion of 
the heart which is first seen is the anterior surface of the right ven- 
tricle ; upward and to the right of this is the right auricle, which 
lies about two-thirds on the right of the sternum and about one-third 
behind it. Its. upper border usually corresponds to the plane of the 
middle of the anterior end of the second intercostal space on the 
right side. Its size varies with the amount of blood which it con- 



26 THE METHOD OF MAKING 

tains. The left auricle lies behind the root of the pulmonary artery, 
so that only its appendix is visible. The middle of the auricle cor- 
responds to the third costal cartilage. Of the left ventricle only a 
narrow rim is seen, on the left side of the right ventricle. The pul- 
monary valve is usually entirely or in part on the left side of the 
sternum, behind the second space or third costal cartilage. 

The aortic valve is usually at the level of the third cartilage or 
the third space, and behind the left two-thirds or half of the sternum. 
The mitral valve is oblique, the upper end to the left. It is on the 
level of the third to the fourth cartilage, near the middle of the 
sternum. The tricuspid is oblique, its upper end to the left ; the 
upper end is at the level of the third cartilage, the third space, or the 
fourth cartilage. The valve is opposite the middle of the sternum. 

The hand should now be passed over the arch of the aorta, to 
ascertain whether or not an aneurism is present. The heart is then 
grasped at the apex, raised out of the pericardium, tilted upward, 
and removed unopened by cutting through the vessels at its base. 

To determine the sufficiency of the aortic and pulmonary valves, 
the heart is held horizontally by both auricles, so as not to pull the 
valves open, and water is poured into the aortic and pulmonary arte- 
ries, and we observe how well the valves support the column of 
liquid. To ascertain the sufficiency of the mitral and tricuspid valves, 
the auricles are first laid open so as to expose the upper surfaces of 
the valves. A large pipe is passed through the aorta or pulmonary 
artery beyond their valves, and a small stream of water allowed to 
flow into the ventricles. The auriculo-ventricular valves will be 
swollen upward, and we can observe their degree of sufficiency. The 
tricuspid valve is normally somewhat insufficient. These water 
tests, however carefully applied, are not very reliable, since under 
the most favorable conditions the natural bearings of the valves are 
not perfectly preserved. 

To ascertain the size of the different valvular openings, we intro- 
duce the fingers, held flat with their sides in contact, into each of the 
orifices, and then measure the width of the fingers at the point where 
they fill the orifice. In this way we find that, under normal condi- 
tions in the adult, the aortic orifice measures about 2.5 cm. (1 in.), 
the mitral valve about 4.5 cm. (1.8 in.), the pulmonary about 3.1 cm. 
(1.2 in.), the tricuspid about 5 cm. (2 in.). 

In order to examine the interior of the heart, we first make an 
incision through the anterior wall of the left ventricle, close to the 
septum, and reaching to the apex of the ventricle; through this 
opening the blade of the enterotome is passed up into the aorta, the 
pulmonary artery being drawn aside with the fingers, and the 
ventricle and aorta are laid open. Vv ith a little care the incision may 



POST-MORTEM EXAMINATIONS. 27 

be made to pass through ODe of the points of junction of the aortic 
valves. 

Clots. — The auricles and ventricles may be empty, or may con- 
tain fluid blood or the so-called heart clots. These heart clots are of 
two kinds — those which are formed some time before death, and those 
which are formed during the last hours of life and after death. The 
clots which are formed some time before death are usually associated 
with organic disease of the heart, especially with dilatation of the 
ventricles. They are firm, dry, and of whitish color ; they may soften 
or be infiltrated with the salts of lime. They are free in the cavities 
of the heart, or entangled in the trabeculae, or firmly adherent to the 
endocardium. They are usually composed of coagulated fibrin. 1 The 
clots which are formed during the last hours of life and after death 
are red, yellow, or white. They may be soft or succulent, or quite 
firm. They may be free in the heart cavities, or be adherent to the 
trabecule, or extend into the large vessels. They are usually most 
constant and of largest size in the right auricle and ventricle. Such 
clots may be formed within two hours after death. Clots of this 
character are a regular post-mortem condition and of no pathological 
significance. It is evident, however, if the blood did coagulate in 
the heart within twenty -four hours before death, that this coagulum 
could not be distinguished from the ordinary post-mortem clots. If 
it is supposed, therefore, that a person dies from heart clot developed 
a few hours before death, the proof of this must be derived largely 
from the clinical symptoms and not from the autopsy. 

The condition of the aortic valves and of the endocardium, and 
the thickness and appearance of the walls of the left ventricle, papil- 
lary muscles, eord?e tendinese, etc., are now noticed. The right ven- 
tricle is now opened by an incision through its anterior wall, close to 
the septum, and examined in the same way. We sometimes see the 
endocardium of the upper part of the left ventricle thick and white 
without the existence of valvular lesions or any clinical history of 
disease. The endocardium and valves are often stained red, par- 
ticularly in warm weather, by imbibition of coloring matter of the 
blood set free by decomposition. To complete the examination of the 
cavities the enterotome is passed into each auricle, carried down 
into the corresponding ventricle, and an incision made along the 
outer border of both auricle and ventricle to the apex of the latter. 
In this way the auriculo- ventricular valves are completely exposed. 

After removing the blood the heart should be finally weighed. In 
adults the normal average weight of the heart is about 292 gm. 
(ibout 10 oz.). The relative weight of the heart to that of the body 

1 For a description of special forms of heart thrombi see p. 501. 



28 THE METHOD OF MAKING 

is in males about 1 : 158-178 ; in females, about 1 : 149-176. Accor< 
ing to Buhl, the average thickness of the wall of the left ventricle ; 
about the middle of the cavity is from 1.6 cm. to 1.7 cm. (from aboi 
f to f in.); of the right ventricle, from 0.4 to 0.6 cm. (from aboi 
i to i in.). 

Generally speaking, the size of the heart corresponds to the si: 
and the development of the individual. In judging of an increase < 
decrease in its size we must consider the weight of the organ and tl 
thickness of its walls. If the person die while the heart is co] 
tracted, the walls of the ventricles will appear thicker, their caviti< 
smaller than usual. If he die of some exhausting disease, lil 
typhoid fever, or if decomposition have commenced, the heart wal 
will usually be flabby and the cavities will appear larger than usua 

Preservation of Specimens. — Parenchymatous and fatty degeneration of the hea 
may be studied microscopically by teasing the fresh muscle in one-half-per-cen.t si 
solution, or by examining in the same solution fresh sections made with the freezii 
microtome, or by hardening small pieces of the muscle in one-per-cent osmic ac 
and teasing in equal parts of glycerin and water. 

The heart valves may be stretched on a flat cork with pins and hardened 
Muller's fluid or alcohol. For the methods of detecting bacteria in ulcerative end 
carditis, see section on Staining Bacteria. When the presence of bacteria is si 
pected cultures should be made and the tissues should be preserved in stroi 
alcohol. 

The Pleural Cavities are next examined. The hand is passe 
into each, and the existence of serous or fibrinous exudations or 
old adhesions ascertained. The method of detecting the presence 
air has been given above. After the commencement of putrefactic 
reddish serum may accumulate in the pleural cavities. This shou 
not be mistaken for the result of disease. 

The Lungs. — Each lung is lifted up in turn, the vessels, etc., i 
its base divided, and the organ removed. If the pleura is vei 
adherent it is better to strip off the costal pleura with the lun^ 
After inspecting the external surface of the lung, observing its siz 
shape, color, and consistence, we open the bronchi. For this purpoi 
we use scissors with long, narrow, blunt-pointed blades, one blade 
little longer than the other. The lung is held in the left hand wi1 
its base upward. We first open the large bronchi which run on tl 
inner side of the lower lobe, afterward those of the upper lob 
Each bronchus should be followed to its smaller ramifications. 

"We should observe the contents of the bronchi and the appea: 
ance of their walls. In the larger and medium-size bronchi the ca 
tilages in their walls do not form complete rings, but appear shinin 
through the mucous membrane like irregular white patches. Th 
appearance should not be mistaken for a pathological change. I 
bodies which have been dead for some time, especially in col 



POST-MORTEM EXAMINATIONS. 29 

weather, the bronchial mucous membrane may be red and swollen 
as a post-mortem change. The contents of the stomach are some- 
times forced, after death, into the pharynx, and thence find their way 
into the trachea and bronchi, giving them a peculiar reddish and 
even gangrenous appearance. Bronchitis does not always leave 
lesions which can be seen after death. 

After the examination of the bronchi the lung is turned over, the 
vessels, etc., at its root grasped with the left hand, and a long, deep 
incision made from apex to base. We observe the appearance and 
texture of the lungs, whether the air vesicles are dilated (emphy- 
sematous) or filled with serum, blood, or inflammatory exudation. 
Fluid can be pressed out of the air vesicles without breaking down 
the lung tissue. Solid inflammatory exudation, on the other hand, 
renders the lung more resistant and easily broken down. Attention 
should be paid to the oozing of purulent or other fluid from the 
smaller bronchi when the lung is squeezed near the cut surface. It 
is the rule to find the lower lobes more congested than the upper. 

Preservation of the Lungs and Bronchi. — If the lungs have been cut, small pieces 
from the affected portions of lung tissue or bronchi should be hardened in Miiller's 
fluid, care being taken not to squeeze or handle them unnecessarily. It is better, 
when the microscopical examination is more important than the macroscopical, not 
to open the lungs at once, but to fill the air spaces with preservative fluid by means 
of a funnel attached to a short rubber tube and canula, which is tied into the main 
bronchus. In this way not only are the minute structures better preserved, but the 
air vesicles are filled out and hardened in an approximately natural condition. Care 
should be taken not to have too great a pressure from the inflowing fluid, since then 
exudations might be displaced or the lung distorted or ruptured. While the lung 
is being filled it should be immersed in a vessel of the same preservative fluid, in 
which it lies for twenty-four hours. It is then cut into small pieces and the hard- 
ening completed. A variety of hardening agents may be used : Strong alcohol, 
Miiller's fluid, or formalin solution (2 : 100) are on the whole the best. If, however, 
the lung is commencing to decay, strong alcohol will stop the process most quickly 
and give as good results as are possible under the circumstances. Alcohol should 
be used when the lungs are to be examined for bacteria. 

It is often desirable, and particularly in cases in which the topography of lesions 
is to be studied, as in acute miliary tuberculosis, acute and chronic phthisis, infarc- 
tions, etc., to inject the blood vessels with colored gelatin. The lung should, after 
the injection, be hardened in alcohol. 

The Pharynx, Larynx, (Esophagus, and Thyroid Gland. — For 
the removal of these parts the incision through the skin should be 
carried upward as far as practicable — when allowable, to a point 
one inch below the chin, the head being allowed to hang backward 
over the edge of the table. 

The soft parts are dissected from the larynx, taking care not to 
cut the thyroid body, and an incision is made through the floor of 
the mouth, following the internal surface of the inferior maxilla. 
Through this incision the fingers are introduced into the mouth, the 



30 THE METHOD OF MAKING 

tongue drawn down, the posterior wall of the pharynx divided abo^ 
the tonsils, and the pharynx and larynx drawn out together. The 
organs are then pulled downward, and with the aid of the knife t] 
trachea and oesophagus are removed entire, the oesophagus being ci 
just above the stomach. If the contents of the stomach are to 1 
preserved, as in cases of suspected poisoning, a ligature is pi 
around the oesophagus just below the point at which it is to be ci 
off. 

With the enterotome the pharynx and oesophagus are now si 
open upon their posterior surfaces. The mucous membrane thi 
exposed is examined for evidences of caustic poisons, of inflamm 
tion, tumors, strictures, etc. The enterotome is next introduced in 
the larynx, and this organ and the trachea laid open along the post 
rior wall. Here we look for oedema of the aryteno-epiglottidea 
folds (oedema of the glottis), for evidences of catarrhal, croupou 
ulcerative, and syphilitic inflammation, and for tumors and lesior 
of the laryngeal cartilages. CElema and redness of the laryn 
may be produced by post-mortsm changes, especially in bodit 
which have been kept for several days in cold weather. A wel 
marked oedema glottidis during life may leave no trace after deatl 
Putrefactive changes usually commence early in the larynx and tn 
chea. 

The thyroid gland is dissected off and examined. Its weigl 
varies a good deal, being, according to Krause, somewhat over c 
gm. (about 1-J oz.). 

Preservation of the Pharynx, Larynx, and Trachea. — These structures are free 
from superfluous tissue and suspended entire by a thread in a large quantity c 
Muller's fluid or alcohol or formalin solution (2:100), in which the hardening] 
completed in the usual way. The cesophagus should be stretched loosely on shet 
cork with pins and hardened in either of the above fluids. The thyroid may be ci 
into small pieces and hardened in Muller's fluid, formalin, or alcohol. The colloi 
material in the acini of the thyroid and in goitres is apt to be preserved withoi 
shrinkage in formalin. 

THE ABDOMEN. 

Returning now to the abdominal cavity, we first dissect off th< 
omentum. If tubercles of the peritoneum exist, they are best seei 
and studied in the omentum. The colon is then raised and dissectec 
free, to the caecum on one side and to the rectum on the other. Th 
colon and small intestines are then drawn first to the right and thei 
to the left side, so as to expose in turn the right and left kidneys 
As each kidney is brought into view an incision is made througl 
the peritoneum over the track of the ureter. The ureter is folio wee 
through its entire length and its condition ascertained. 



POST-MORTEM EXAMINATIONS. 31 

The Kidneys are then removed, separating the peritoneum and 
fat from them with the hand, and dividing the vessels with the knife. 
The suprarenal capsules, which are attached to the upper end of 
each kidney, are removed at the same time. The kidneys may be 
softened by putrefaction, or the surface may have a greenish-gray 
color caused by the post-mortem action of putrefactive gases on the 
haemoglobin. 

An incision is made through the capsule, along the convex bor- 
der of the kidney, and the membrane stripped off. We notice the 
degree of adherence of the capsule to the kidney, and also the sur- 
face of the latter, whether smooth or roughened, pale, congested, or 
mottled ; an incision is made along the convex surface down to the 
pelvis, so that the organ is divided into halves. "We observe the re- 
lative thickness of the cortical and pyramidal portions, as well as 
the size of the entire organ. To ascertain the latter point, it is well 
to weigh each kidney ; the normal weight is from 130 to 150 gm. 
(about 4| to 5 oz.). 

It is necessary to remember, however, that in a kidney which is 
much atrophied there may be an increase of fat in the pelvis, which 
gives the organ nearly its normal size and weight, while the kidney 
tissue proper may have in great measure disappeared. 

The weight of the kidneys of adults is given by Vierordt in gene- 
ral as about 0.48 per cent of that of the entire body. 

We now inspect the kidney tissue more closely, especially the 
cortical portion. The pyramids consist largely of tubes running in 
nearly straight lines from the apex to the base of each pyramid. 
These straight tubes pass from the pyramids into the cortex in 
bundles, called medullary rays, many of them retaining their straight 
course until they nearly reach the surface of the kidney. These 
straight tubules send off branches on all sides of the rays, which 
become convoluted, from Henle's loops, and finally terminate in the 
glomeruli or Malpighian bodies. In this way the cortex of the 
kidney, as seen in section, is divided into alternate bands of straight 
tubes, convoluted tubes, and glomeruli; both sets of bands being 
perpendicular to the surface of the kidney, and called respectively 
medullary rays and labyrinths. About the convoluted tubules and 
glomeruli is a rich venous plexus; and since after death the blood 
usually remains in this plexus and in the glomeruli, the bands con- 
taining the convoluted tubules, i.e., the labyrinths, usually appear 
red, while the medullary rays are grayish-white. In a normal 
kidney, therefore, the cortex should be regularly striped in narrow 
alternating red and whitish bands. 

The average thickness of the cortex of the kidney is about one- 
third of an inch. 



32 THE METHOD OF MAKING 

If there be extensive congestion the entire cortex is red. If the 
epithelium of the tubules degenerates and fills them up, or if there 
are considerable changes in the interstitial tissue, the regular bands 
are lost and the cortex is irregularly mottled. If the tubular epithe- 
lium becomes filled with fat globules, this is indicated by an opaque 
yellow color of the affected parts ; in many cases, therefore, the ex- 
istence of kidney disease can be recoguized with the naked eye. 

If waxy degeneration be present to a marked extent, it may be 
manifest by a peculiar translucent appearance of the affected parts, 
but in most cases it is necessary to apply reagents to demonstrate it 
satisfactorily. The cut surface of the kidney is washed with water 
to free it from blood, and repeatedly brushed with an aqueous solu- 
tion of iodine (iodine 1 part, potassium iodide 3 parts, water 100 
parts). The glomeruli and the blood vessels are most frequently 
affected, and, if so, they may appear as mahogany -colored dots and 
lines on a yellow ground. 

But this reaction is not constant, and for accurate detection of 
amyloid substance recourse shall be had to other reagents applied to 
sections of the hardened tissues (see page 101). 

The pelvis of the kidney should be examined for inflammatory 
lesions and calculi. Sometimes a whitish fluid is seen in the pelvis 
and can be squeezed from the papillae; this is produced by a post- 
mortem desquamation of the epithelium, but is liable to be mistaken 
for pus. 

Preservation of the Kidney. — If the kidney be not opened the blood vessels may be 
injected through the renal artery, slowly and under a low pressure with formalin 
solution (2 : 100) , or with Mtiller's fluid, or with eighty-per-cent alcohol. Afterfilling 
the vessels with either of the above fluids they are tied, and the entire organ is placed 
in a large quantity of the injecting fluid for twenty-four hours. The kidney is then 
cut into small pieces and the hardening is completed in the usual way. 

In most cases, however, the kidneys will have been opened for inspection at the 
autopsy. Then small pieces are removed from the various regions and hardened in 
alcohol or formalin or Mtiller's fluid. 

For special cell studies osmic acid, sublimate, and other hardening agents may be 
used. 

Kidneys which are to be examined for the presence of bacteria should be cut into 
small pieces and placed at once in strong alcohol, which should be changed once or 
twice, and in which they are permanently preserved. 

The Suprarenal Capsules are in the foetus of an ovoidal, in the 
adult of a triangular shape. They are situated at the upper and 
inner border of the kidney, to which they are loosely attached by 
connective tissue. On the anterior surface is an irregular fissure, 
called the hilus, from which the veins emerge. The size varies con- 
siderably, but in the adult the average vertical diameter is from 3.2 
cm. (li in.) to 4.5 cm. (If in.), the transverse diameter about 3.2 cm. 



POST-MORTEM EXAMINATIONS. 33 

(1^ in.), and they are from 4.2 mm. (-J-in.) to 6.4 mm. (i in.) in 
thickness. They weigh in the adult from about 4 gm. (1 3 ) to 8 
gm. (2 3 ). They are composed of a cortical and medullary portion, 
the cortex forming a yellowish shell around the dark-red or brown 
medulla. They are enclosed in a connective-tissue capsule, from 
which fibrous processes extend inward, dividing the gland in a series 
of irregular chambers. Those in the cortex are mostly elongated, 
giving this portion a striated appearance, while those in the medulla 
are polyhedral. It is in these spaces that the parenchyma cells lie. 
The suprarenal capsules readily decompose; the inner layer of the 
cortex may soften and break down, so that the outer zone forms a 
sort of cyst filled with reddish-brown broken-down substance. Hy- 
pertrophy, tuberculosis and cheesy degeneration, fatty degeneration, 
and tumors are to be looked for. 

Preservation. — The suprarenal capsules should be hardened in Miiller's fluid, in 
formalin solution (2 : 100), or in strong alcohol. 

The Spleen. — This organ has, when removed from the body, the 
general shape of a flattened ellipsoid, most curved on its external and 
posterior surface. It is situated in an oblique position on the left 
side of the stomach, and between its cardiac end and the diaphragm. 
The vessels are given off from its inner surface, which is crossed by 
a more or less well-marked vertical ridge. The point of emergence 
of the vessels is called the hilus. Its long diameter extends from the 
seventh intercostal space to the eleventh rib. Its upper portion is 
separated from the ribs by the lungs ; its lower portion by the dia- 
phragm. 

Its usual length in the adult is, according to Yierordt, from 12 to 
13 cm. (about 4f to 5 in.) ; its breadth from 7 to 8 cm. (about 2f to 
3 in.); its thickness 3 cm. (about \\ in.). Its average weight is 
about 171 gm. (about 7 oz.). The dimensions of the spleen as given 
by Krause are somewhat greater than the above. But its measure- 
ment and weight vary considerably within the limits of health. It 
is in these respects the most variable organ in the body. In old age 
the average weight gradually diminishes. 

The spleen is enclosed in a fibrous capsule covered with perito- 
neum. The parenchyma is formed of blood vessels and fibrillar con- 
nective tissue, and of a soft, dark-red pulp in which are embedded 
whitish spheroidal or elongated bodies, the glomeruli or Malpighian 
bodies. In the normal human spleen the glomeruli are hardly per- 
ceptible to the naked eye, but sometimes they are very plain. Some- 
times the fibrous stroma is very apparent, sometimes not. 

The size, consistence, and color of the organ vary a good deal 
without any known cause. Decomposition softens it. Thickenings 
4 



34: THE METHOD OF MAKING 

of the capsule and abnormal adhesions are very common, and often 
occur without any clinical history indicating disease. We should 
look for changes in size, pigmentations, hyperplasia of the connec- 
tive tissue, amyloid degeneration, tubercles, and infarctions. 

Not infrequently one or more spheroidal or flattened so-called ac- 
cessory spleens are found in the vicinity of the spleen ; they vary in 
size from that of a pea to that of a walnut. 

Preservation. — In certain diseases of the pulp, leukaemia, leucocythaemia, etc, the 
tissue should be teased, when fresh, in one-half -per- cent salt solution, or examined 
by the staining methods described under the lesions of the blood. For general pur- 
poses small pieces of the organ are hardened in Matter's fluid or alcohol. 

The Intestines. — The rectum is divided, the intestine seized 
with the left hand, and, being kept stretched, is separated from its 
attachments by repeated incisions through the mesentery close to 
the gut, until the duodenum is reached, where it is again cut off. 
The operation is more cleanly if, before dividing the gut, ligatures 
are placed around it at either end. The entire length of the gut 
is now laid open with the enterotome along the mesenteric attach- 
ment, the mucous membrane is cleaned with a stream of water and 
then examined. 

In cases of suspected poisoning a ligature should be placed 
around the rectal end of the gut and two around the duodenal end, 
and it is then cut off below the former and between the latter liga- 
tures. The gut is now opened and the contents emptied into a clean 
glass jar for delivery to the chemist, care being taken that they be 
not allowed to touch anything but the inner surface of the jar. 
After washing the intestine in pure fresh water and examining it, 
it should be placed entire in another clean jar and sealed. 

Cadaveric lividities are very common in the intestines, and are 
usually most marked in the dependent portions. They are apt to 
occur in patches, but may be diffuse and very extensive. If the 
wall of the gut be stretched they are often seen to be discontinuous, 
owing to the pressure of the blood from the parts which are squeezed 
by folds. Small patches of arborescent or diffuse red staining are 
often seen, formed by the imbibition from the vessels of decompos- 
ing haemoglobin. In the more advanced stages of decomposition the 
mucosa may be softened and loosened. A dark purple or brownish 
discoloration of the entire intestinal wall is frequently seen, either 
diffuse or in patches. Much experience and careful observation are 
requisite in forming a correct judgment regarding the significance 
of changes of color in the intestines. Caution is necessary in distin- 
guishing normal digestive hyperaemia from abnormal congestion. 
A very considerable congestion may exist without disease. In chol- 



POST-MORTEM EXAMINATIONS. 35 

era seasons especially, observers are prone to call the most moderate 
degree of congestion abnormal. 

The lesions ordinarily to be looked for are catarrhal, croupous, 
and ulcerative inflammations, perforations, haemorrhages, strictures, 
tumors, amyloid degeneration, swelling and ulceration of the solitary 
follicles and Peyer's patches, and pigmentation. For the detection 
of amyloid degeneration of the mucosa this structure should be care- 
fully washed and brushed with a solution of iodine (see p. 32). 

Preservation. — For the general purposes of microscopic study portions of the gut 
should be gently stretched on cork (the mucosa side free) and placed for a few 
minutes in strong alcohol, and then transferred to eighty -per-cent alcohol, in which 
the hardening is completed. The transfer to weaker alcohol is to prevent the speci- 
men from becoming brittle. Formalin solution (2 : 100) may also be used for harden- 
ing the mucous membrane, the process being completed by alcohol. 

For obvious reasons the mucous membrane should be handled as little as possible, 
for, in the majority of cases, decomposition and softening have already set in at 
the time of the autopsy, and, under the most favorable conditions, the epithelium is 
very easily rubbed off. 

In cases in which the most perfect preservation of the topographical features, as 
well as the minute structure of the intestinal mucosa, is desirable, even at the ex- 
pense of an inspection of the fresh tissue, another mode of procedure is to be recom- 
mended. 

Selected segments of the gut are, after removal from the body, allowed to re- 
main unopened on the table while ligatures are tied around the ends. The isolated 
segments, or the whole gut, are now to be moderately filled — not distended — with 
strong alcohol by means of a syringe with a needle canula ; or one end of the seg- 
ment may be tied and the alcohol introduced through a funnel at the other, which is 
then ligated. The segments to be preserved should now be placed unopened in 
strong alcohol. After twenty -four hours they may be opened with scissors or a 
sharp knife, cut into suitable pieces, and kept permanently in eighty-per-cent alco- 
hol. Intestinal contents maybe washed out with alcohol before filling the gut. For- 
malin (2 : 100) may be used instead of alcohol for the preliminary hardening. 

Powers has found that an excellent preservation of a portion of the intestinal 
mucous membrane may be obtained even when the autopsy is postponed for a con- 
siderable time after death, by the injection of two-per-cent formalin directly into the 
intestine per anum, shortly after death. 

At the autopsy the tissues are removed and the hardenings completed in the 
usual way. 

The Stomach and Duodenum. — We now introduce the entero- 
tome into the duodenum at its transverse portion, and open it on the 
convex border. When the pylorus is reached the incision is carried 
obliquely over to the greater curvature of the stomach, along which 
it is extended as far as the oesophageal opening, and the organ 
examined in situ ; or, if a more careful examination of the stomach 
is called for, after ascertaining whether or not the bile duct is per- 
vious (see below), the duodenum and stomach may be removed to- 
gether, and the stomach opened and examined on the table. If 
poisoning be suspected a ligature should have been placed, earlier in 



36 THE METHOD OF MAKING 

the examination (see above), around the lower end of the oesophagu 
and the duodenum. The stomach and duodenum are now remove 
together unopened. They are to be opened in a carefully cleanse 
glass jar, and after an inspection of the mucous membrane and th 
contents with the naked eye and a hand lens, stomach, duodenun: 
and contents are to be sealed in the jar for the chemist. 

We now look for the orifice of the bile duct, which will be f oun 
about the middle of the descending portion of the duodenum on it 
concave border. Pressure on the gall bladder or on the commo 
duct will usually cause the bile to flow into the intestine if the duct 
are pervious. But a sufficient degree of stoppage may exist in th 
ducts to give rise to marked symptoms of disease without preventin 
the flow of bile under these conditions, even with a moderate pressure 
A long director is now passed into the gall duct, which is laid coir 
pletely open ; ulcerations, cicatrices, gall stones, inflammatory It 
sions, and tumors are looked for. In stricture of the gall duct th 
mucous membrane above will often be found bile-stained, while bt 
low it is colorless. At this point, should there be any special reasoi 
for doing so, the portal vein, which lies close behind the ductus chc 
ledochus, should be opened and examined for periphlebitis, phlebitis 
and thrombosis. The mucous membrane of the duodenum and stc 
mach are now rinsed off and examined. Acute inflammations fror 
caustic poisons, chronic catarrhal inflammations, haemorrhages, uJ 
cers, erosions, swelling of the solitary follicles (lymph nodules), am 
tumors are lesions most frequently seen. We sometimes find a dif 
fuse congestion of the stomach similar to that produced by irritan 
poisons, as a result of doses of croton oil given just before death. 

Preservation. — The same methods should be used as for the intestines (see above 
Tumors should be cut into small pieces and hardened in Muller's fluid. 

The Liver. — To remove the liver, the diaphragm is first divide* 
on one side, of the suspensory ligament as far back as the spine ; th 
suspensory ligament is then divided ; then the right and left lobe 
being in turn raised, the lateral ligaments are severed. Then, seizin| 
the left lobe, the organ is dragged obliquely downward into the ah 
dominal cavity, the remaining attachments being dissected away 
The liver is first laid on its superior surface and the gall bladder am 
its contents examined. The character of the gall is to be determined 
and gall stones, inflammatory lesions, and tumors sought for. T 
determine the actual size of the organ, it should be both measure( 
and weighed. Its size varies greatly in different healthy individuals 
but in general it may be said that it measures from 25 to 30 cm. (1( 
to 12 in.) transversely, from 15.3 to 18 cm. (7-£ to 9 in.) anterc-poste 
riorly, and about 12 cm. (6 in.) at its thickest part; the ordinary 



POST-MORTEM EXAMINATIONS. 3? 

bulk is about 229 to 252 c.c. (90 to 100 cu. iu.) ; its ordinary weight 
between 1.550 to 1,860 gm. (50 to 60 oz.). In children its weight 
relative to that of the body is greater than in adults. The liver is 
increased in size and weight during digestion and by congestion 
from any cause. 

The surface of the liver is now examined, and it is then laid on 
its lower surface and several deep incisions made from the convex 
surface downward. The color and consistence of the liver tissue 
should be noticed, also the distinctness with which the lobular out- 
lines can be seen ; wmether or not the centres of the lobules are con- 
gested or their peripheries lighter in color than usual ; the presence 
of tumors, tubercles, abscess, ecchinococcus, new connective tissue, 
and pigmentation. Suspected amyloid degeneration should be tested 
for by the iodine solution (p. 32). 

We often find the surface of the liver of a greenish or very dark- 
brown color ; less frequently the same color extends into the sub- 
stance of the organ. This discoloration, which is entirely post- 
mortem, is, like the similar discoloration of other internal organs, 
produced by the. action of the gases of putrefaction on the coloring 
matter of the blood. 

Preservation. — For the study of parenchymatous degeneration, sections of the 
fresh frozen tissue or small teased fragments should be examined in half-percent 
salt solution. For general purposes small pieces should be hardened in Muller's 
fluid or in formalin solution (2 : 100) or in alcohol. Tumors should be treated in the 
same way. In many cases of marked cirrhosis the topography of the lesion is best 
demonstrated by injecting the organ with blue gelatin through the portal vein and 
then hardening in strong alcohol. 

The Pancreas. — This organ, of a light yellowish-red color, is 
elongated, irregularly prismatic in shape, and flattened antero-pos- 
teriorly ; the right end, called the head, is broader than the rest 
and lies in the concavity of the duodenum. The remainder of the 
organ, the body and tail, are usually tapering and lie transversely 
in the abdominal cavity, the tail reaching to the spleen. Its size 
and weight vary considerably ; its usual length is from 15.3 to 20.3 
cm. (6 to 8 in.); its breadth about 3.8 cm. (l£ in.); its thickness 
about 1.3 to 2.5 cm. (} to 1 in.); its weight is usually from 70 to 108 
gm. (2i to 3-j- oz.). The organ may be rounded instead of flattened ; 
the head and tail may be disproportionately large ; the tail may be 
unusually long or may be divided or curved. The superior mesen- 
teric artery and vein, which pass behind the gland, are usually partly 
embedded in it, but are sometimes completely enclosed. 

A longitudinal incision should be made through the whole gland, 
which may remain in situ, and its substance and duct should be 
searched for calculi, tumors, malformations, and evidences of acute 
and chronic inflammation, fat necrosis, and amyloid degeneration of 



38 THE METHOD OF MAKING 

the blood vessels. The pancreas is frequently of a dark-red color 
from post-mortem staining. 

Preservation. — Portions of this organ should be hardened in strong alcohol, or in 
formalin or sublimate solution. 

THE GENITO-URINARY ORGANS. 

The Male Organs. — If the urine is to be examined it may be 
drawn off with a catheter ; or a vertical incision may be made into 
the bladder just above the symphysis pubis, and some of the urine 
dipped out. The cut end of the rectum should now be grasped with 
the left hand and raised up, and this and the bladder, prostate 
gland, etc. , dissected away from the pelvis, the knife being carried 
close to the bone. The bladder is now drawn backward and the 
loose tissue close under the symphysis pubis cut. The body of the 
penis is then shoved backward within the skin and dissected away 
from behind beneath the symphysis, and finally cut off just behind 
the glans penis. The penis and bladder are now drawn backward 
and upward, and the pelvic organs removed together. Or, the penis 
may be removed by sawing away the bones above the pubic arch, 
and then dissecting away the penis, whose root is thus exposed. 

The pelvic organs are then laid on the table, the bladder upper- 
most ; a long director is passed into the urethra, which is opened on 
its upper surface through its entire length, and the bladder widely 
opened. In the urethra the presence of strictures, diverticulae, 
ulcers, inflammatory lesions is to be noticed ; in the bladder inflam- 
matory lesions, hypertrophies, congestion and ecchymosis of the 
mucous membrane, hyperplasia and ulcers of the lymph nodules, 
and tumors. The organs are now turned over ; the rectum opened 
and examined for varicose veins, haemorrhages, ulcers, strictures, 
and tumors. The prostate gland is then cut into and the presence 
of calculi, inflammatory lesions, hypertrophies, and tumors sought 
for. Lastly, the vesicular seminales are examined, in which, though 
rarely, we may find evidences of tubercular inflammation and dila- 
tation. 

The Testicles may be removed, when necessary, without cut- 
ting the scrotum, by enlarging the inguinal canals from within and 
crowding the glands through them and cutting them off. The 
average weight of the adult testicle with its epididymis is, accord- 
ing to Krause, from 15 to 24.5 gm. (about f oz.). Inflammatory 
lesions, tuberculosis, abscesses, and tumors are the most frequent 
lesions. 

Preservation. — The urethral canal and bladder may be pinned open and hardened 
in strong alcohol, or in formalin solution, or in Muller's fluid. The prostate, vesic- 
uke seminales, testicles, and tumors may be hardened in the same fluids. 



POST-MORTEM EXAMINATIONS. 39 

The Female Organs. — The position and general condition of the 
pelvic organs should first be determined by inspection. Abnor- 
mal adhesions of the ovaries, broad ligaments, Fallopian tubes, and 
uterus ; malpositions of the uterus ; subserous tumors of the uterus, 
and ovarian tumors, are frequently observed. Hsemorrhage into 
the posterior cul-de-sac is sometimes found. The urine should be 
collected, if necessary, as above directed • the organs should be dis- 
sected away laterally, as in the male, care being taken not to injure 
the ovaries and Fallopian tubes. The bladder is then drawn strongly 
backward and upward, and dissected away from the symphysis and 
the pubic arch, and, the point of the knife being carried forward 
and downward, the vagina is cut off in its lower third, the rectum 
severed just above the anus, the remaining attachments cut, and 
the pelvic organs taken out together. If it be necessary to remove 
the external generative organs, after freeing the lateral surfaces of 
the internal organs and the bladder, the legs are widely separated 
and the vulva and anus circumscribed by a deep incision. The 
tissues close beneath the pubic arch are now dissected away from 
below and the vulva thrust back beneath the symphysis ; it is now 
seized above the bone, and together with the anus dissected away 
and removed with the other organs. 

The Bladder is first opened and examined. The vulva may now 
be examined for hypertrophies, inflammatory lesions, ulcers, cica- 
trices, cysts, and tumors. The vagina is opened along the anterior 
surface ; its more common lesions are inflammations, fistulse, ulcers, 
tumors, and rarely cysts. 

The Uterus. — Before opening this organ its size and shape 
should be determined. The adult virgin uterus is a pear-shaped 
body, flattened antero-posteriorly ; the upper portion, or body, is 
directed upward and forward, whilst the lower portion, the cervix, is 
directed downward and backward. It is covered anteriorly by peri- 
toneum to a point a little below the level of the os internum ; pos- 
teriorly, to a point a little below the level of its junction with the 
vagina. The peritoneal investment separates from the organ at the 
sides to form the broad ligaments. The uterus is held in position 
by the broad and round ligaments and by its attachments to the 
bladder and rectum and vagina. The upper end, the fundus, does 
not extend above the level of the brim of the pelvis. Its average 
length is about 7.6 cm. (3 in.) ; its breadth about 5.1 cm. (2 in.) ; its 
thickness about 2.5 cm. (1 in.) ; its average weight is about 31 to 46 
gm. (1 to 1| oz.). During menstruation the uterus is slightly 
enlarged and the mucous membrane of the body becomes thicker, 
softer, and its vessels engorged with blood ; while its inner surface is 
more or less thickly covered with blood and cell detritus. A descrip- 



40 THE METHOD OF MAKING 

tion of the complicated changes in the uterus which pregnancy entails 
may be found in the works on obstetrics. After pregnancy the 
uterus does not return to its original size, but remains somewhat 
larger ; the os is wider and frequently fissured. 

We not infrequently find in the mucous membrane of the lower 
part of the cervix small transparent, spheroidal structures, called 
ovula Nabothi ; these are small retention cysts caused by the closure 
of the orifices of the mucous glands of the part. The more common 
lesions observed in the uterus are malpositions, malformations, 
lacerations, ulcerations of the cervix, acute and chronic inflammation 
of the mucous membrane or muscularis, or both, thrombosis and 
inflammation of the veins, and tumors. 

In the infant the uterus is small, the body flattened, the cervix 
disproportionately large. During childhood the organ increases in 
size, but the body remains small in proportion to the cervix. At 
puberty the shape changes and the body becomes larger. 

The Ovaries are flattened, ovoidal bodies, situated one on each 
side and lying nearly horizontally at the back of the broad ligament 
of the uterus. Their siz3 is variable and they are usually largest in 
the virgin state. Their average weight is from 3.9 to 6.5 gm. (3 to 
5 3). They measure about 3.8 cm. (LJ in.) in length, 1.9 cm. 
(f in.) in breadth, and nearly 1.3 cm. (^ in.) in thickness. The sides 
of the ovary and its posterior border are free ; it is attached along 
the anterior border ; to its end is attached the ovarian ligament ; to 
its outer extremity one of the fimbriae of the Fallopian tube. The 
ovary is covered on its free surface by cylindrical epithelium, and its 
surface is less glistening than the general peritoneum. The surface 
of the ovary is smooth in the young, but becomes rougher and 
depressed in spots as the process of ovulation goes on. In adult 
females we usually find corpora lutea in their various stages. We 
should seek for evidences of acute and chronic inflammations, for 
tumors and cysts. 

The Fallopian Tubes, lying in the upper margin of the broad 
ligaments, are from 7. 6 to 10 cm. (3 to 4 in. ) in length. The length 
often differs considerably on the two sides. They commence at the 
upper angles of the uterus as small perforated cords, which become 
larger further outward and bend backward and downward toward 
the ovary. They terminate in an expanded fimbriated extremity 
about 2.5 cm. (1 in.) beyond the ovary. They are covered by peri- 
toneum, and the mucous membrane lining them, continuous with that 
of the uterus, is thrown into longitudinal folds. Malpositions by 
adhesions, closure, inflammations, and cysts are the more common 
lesions. The possibility of tubal pregnancy should be borne in 
mind. 



POST-MORTEM EXAMINATIONS. 41 

Preservation. — All of these organs and their tumors may be hardened in Muller's 
fluid, or in formalin solution, or in strong alcohol. The vagina should be stretched 
flat on cork and the cavity of the uterus laid wide open. Great care should be taken 
not to touch either the internal surface of the uterus or the external surfaces of the 
ovaries, since in both the epithelium is very easily rubbed off. 

It is better, after opening them by a transverse incision, to suspend the ovaries 
by a thread in a jar of the preservative fluid than to let them lie on the bottom, 
since the epithelium is thus less liable to be rubbed off. Larger cysts of the ovary 
for exhibition purposes should be distended with preservative fluid (see p. 64). 

AUTOPSIES IN MEDICO-LEGAL CASES. 

While every autopsy should be made as carefully and complete^ 
as circumstances will permit, it should be always borne in mind that 
in examinations which may have medico-legal bearings it is of the 
highest importance to examine thoroughly both macroscopically and 
microscopically every part of the body from which light may be 
derived as to the cause of death, for in medico-legal cases it is not 
infrequently as important to be able by a complete examination to 
declare the absence of lesions which could cause death as to deter- 
mine the presence of those upon which the opinion as to the actual 
cause of death in a particular case rests. Bearing this in mind, the 
technique of autopsy making is essentially the same whatever the 
ends which the facts elicited may be destined to serve. 

AUTOPSIES IN CASES OF SUSPECTED POISONING. 

It is always best, in cases of suspected poisoning, to preserve for 
ihe chemist not only the stomach and intestine, but the entire liver 
and brain ; or, if portions of these only can be saved, these portions 
should be carefully weighed, as well as the entire organs, and the 
relative amount of tissue reserved carefully noted at the time. It is 
even well, particularly in cases in which the administration of the 
readily diffusible poisons, such as arsenic, strychnia, etc., is sus- 
pected, to preserve the whole of all the internal organs, together with 
a large piece of muscle and bone; since with large quantities of 
tissue the results of the chemical analysis depend less upon calcula- 
tions, and are hence more comprehensible to the average jury. In 
all such cases jars should, if possible, be procured which have never 
been used before, and these should be carefully washed and rinsed 
with distilled water. They should have glass stoppers and be sealed 
at once and carefully labelled before leaving the hands of the operator. 
If they can be delivered to the chemist without much delay, 
no preservative fluid should be added. II they are to be kept for 
a considerable time, pending the action of a coroner's jury or for 
some other reason, a small quantity of pure strong alcohol may be 



42 THE METHOD OF MAKING 

poured over them. In this case the operator should be particular 1 
preserve a quantity, at least half a pint, of the specimen of alcoh. 
used, in a clean, sealed, and labelled bottle, so that this may be teste 
by the chemist and be proven to be free from the poison. It is betfc 
in all cases, however, to avoid, if possible, the use of alcohol. In a 
autopsies which may have medico-legal importance full notes shou] 
be taken by an assistant as the operation proceeds, carefully rea 
over immediately afterward, and dated and kept by the operator f( 
future reference. The labelling and disposition of the jars should I 
recorded in the notes. The specimens should not for a moment I 
out of the sight of the operator until they are placed under lock an 
key and seal, or are delivered to some authorized person, so that the] 
may be no question of their identity should the case come into cour 



EXAMINATION OF THE BODIES OF NEW-BORN 

CHILDREN. 

In examining the bodies of new-born children we may have 1 
determine, besides the ordinary lesions of disease, the age of tl 
child, whether it was born alive, how long it has been dead, wtu 
was the cause of death. 

GENERAL INSPECTION. 

The Size and Age. — Caspar 1 gives the following description < 
the foetus during the different months of intra-uterine life : 

At the fourth week the embryo is 8 to 13 mm. ( T \ to -£$■ in.) lon| 
The cleft of the mouth and two points indicating the eyes can I 
recognized in the head. The extremities are represented by litt' 
wart-like projections. The heart can be distinguished ; the liver 
disproportionately large. The umbilical vessels are not yet f ormec 
The entire ovum has about the size of a walnut. 

At the eighth week the embryo is 2.3 to 4 cm. ( T 9 ¥ to 1 T V in.) lon^ 
The head forms more than a third of the entire body ; the mouth : 
very large ; the nose and lips can be distinguished, but not the ei 
ternal ear. The hand is longer than the forearm ; the fingers ai 
formed, but joined together ; the toes look like little buds ; the sok 
of the feet are turned inward. The position of the anus is indicate 
by a point. The abdomen is closed. All the viscera can be reco£ 
nized. Centres of ossification are formed in the apophysis of the fin 
cervical vertebra, the humerus, radius, scapula, ribs, and cranig 
bones. There are rudimentary external genitals, but the sex ca 

1 Caspar, "Handbook of Forensic Medicine." Revised German Edition by Limai 
or Sydenham Society Translation. 



POST-MORTEM EXAMINATIONS. 43 

hardly be distinguished. The ovum has about the size of a hen's 
egg. 

At the twelfth week the placenta is formed. The embryo is 5 to 

6.5 cm. (2 to 2-J- in.) long and weighs about 31 gm. The head is 
separated from the thorax by a distinct neck. The eyes and mouth 
are closed. The nails can be perceived on the fingers. The sex can 
be recognized. The umbilical cord is inserted near the pubes ; the 
muscles begin to be recognizable. The thymus and suprarenal cap- 
sules are formed. The cerebrum, cerebellum, medulla, and the cav- 
ities of the heart can be recognized. The humerus is 1.7 mm. long ; 
the radius 5.5 mm.; the ulna 6.6 mm.; the femur and tibia 4.4 to 

6.6 mm. ; the fibula 5.5 mm. The ovum is as large as a goose's egg. 
At the sixteenth week the embryo is 13 to 15 cm. (5 to 6 in.) long 

and weighs 77 to 93 gm. (2 J to 3 oz). The skin is of a rose- red color 
and has considerable consistence. The formation of fat in the 
subcutaneous tissue has begun. The scrotum and labia are formed. 
The face begins to assume its characteristic appearance. There is 
whitish meconium in the duodenum. The liver is not so dispropor- 
tionately large, and the gall bladder is formed ; the anus is open. 
The length of the humerus, radius, and ulna is 1.7 cm. ; the femur 
and tibia 8.8 to 11 cm. The calcaneus begins to ossify at the middle 
of the fourth month. 

At the twentieth week the embryo is 26 to 28 cm. (10 to 11 in.) 
long ; it weighs from 225 to 320 gm. (7 T V to 10 oz.). The nails are 
quite perceptible. There is a thin down on the head. The head 
is still disproportionately large, occupying about one-fourth of the 
body. There is as yet none of the vernix caseosa. The secretion of 
bile has commenced and stains the meconium. The insertion of the 
umbilical cord is still further off from the pubes. The liver, heart, and 
kidneys are large in proportion to the other organs. The convolu- 
tions of the brain cannot be recognized. The humerus is 2.8 to 3 
cm. long; the radius 2.6 cm.; the ulna 2.8 cm.; the femur, tibia, 
and fibula, each 2.6 cm. The astragalus and the upper part of the 
sternum begin to ossify. 

From this time on the length of the foetus forms an approxi- 
mately accurate basis for the estimation of its age. From this pe- 
riod till its maturity the length of the foetus, determined in 
centimetres, corresponds to about one-fifth of the number of 
months of its age. From this time on the weight exhibits marked 
individual differences, and is therefore a less reliable criterion of its 
age than is the length. 

At the twenty-fourth week the embryo is 31 to 34 cm. (12 to 13 
in.) long and weighs 750 to 875 gm. (24 to 28 oz.). The lanugo and 
vernix caseosa are formed. The skin is of a dusky cinnabar-red 



44 THE METHOD OF MAKING 

color. The meconium is darker. The scrotum is empty, small, anc 
red ; the labia majora are prominent and held apart by the project 
ing clitoris. The pupillary membrane is present and readily recog 
nized. The length of the humerus and radius is 3.5 cm. ; of the ulna 
femur, tibia, and fibula, each 3.7 cm. 

At the twenty-eighth week the embryo is 36.4 to 39 cm. (14i to 15; 
in.) long and weighs 1,500 to 1,750 gm. (48 to 57 oz.). The hair ii 
more abundant and longer. The great fontanelle measures about 
cm. (l-|in.) in diameter, and all of the fontanelles are readily per 
ceived. The skin is of a dirty-reddish color and abundantly bese 
with the lanugo and vernix caseosa. The large intestine contain 
much meconium. The humerus is 4.5 to 5 cm. long; the radius 3. 
cm.; the ulna 4 cm.; the femur, tibia, and fibula, each 4.2 to 4. 
cm. 

At the thirty-second week the embryo is 39 to 41.5 cm. (15i t 
16.i in.) long and weighs 1,500 to 2,500 gm. (48 to 81 oz.). The ski: 
is lighter in color ; the pupillary membrane has disappeared. Th 
testicles are in the scrotum or the inguinal canal ; the labia are sti' 
widely apart and the clitoris prominent. The nails reach nearly t 
the ends of the fingers. The humerus is 5 to 5.2 cm. long; the ra 
dius 4 to 4.2 cm. ; the ulna 4.8 to 5 cm. ; the femur 5.2 cm. ; the tibi 
and fibula, each 4. 8 to 5 cm. The last sacral vertebra begins to o^ 
sify. 

At the thirty-sixth week the embryo is 44.2 to 46 cm. (17.4 to 1 
in.) long and weighs about 3,000 gm. (97 oz.). The scrotum begin 
to become wrinkled and the labia to close. The hair becomes mor 
abundant, while the lanugo begins to diminish in amount. 

At the fortieth week the foetus is fully developed and the ten 
of its intra-uterine life accomplished. 

The fresh corpse of a new-born child at term no longer resemble 
that of the immature foetus. The skin is firm and pale, like that c 
an adult. The lanugo has disappeared except on the shoulders. I 
the majority of cases the hair on the head is 1.5 to 2 cm. (f to \ in. 
long. The great fontanelle is, in the average, 2 to 3 cm. ( T 8 ¥ to 1-j 
in.) long. As determined by an analysis of 661 cases, the averag 
length is 50 cm. (20 in.), the weight 3,256 gm. (105 oz.). The nail 
are hard and reach to the tips of the fingers, but not to those of th 
toes. The cartilages of the ears and nose are hard. The labia ar 
more nearly closed. An ossification centre in the lower epiphysis c 
the femur should be sought for, as its presence is one of the mos 
reliable signs of the maturity of the foetus. If it is absent the fcetu 
is, as a rule, not more than thirty-seven weeks old ; but in rare case 
it may be absent at term. A centre of ossification 1 mm. (.039 in. 
in diameter indicates an age of 37 to 38 weeks, if the child was bor] 



POST-MORTEM EXAMINATIONS. 45 

dead or died soon after birth. Rarely it is no larger than this at 
term. A diameter, at birth, of 1.5 to 9 mm. (.058 to .351 in.) indi- 
cates an age of 40 weeks. A diameter of less than 9 mm. (.351 in.) 
indicates, as a rule, that the child has lived some time after its birth; 
a less diameter than 7 mm. (.273 in.), however, does not prove the 
contrary, 

Twenty-four hours after the birth of the child the skin is firmer 
and paler. The umbilical cord is somewhat shrivelled, although still 
soft and bluish in color. From the second to the third day the skin 
has a yellowish tinge and the cuticle sometimes appears cracked. 
The umbilical cord is brown and dry. From the third to the fourth 
day the skin is yellower, and the cuticle is apt to separate from the 
skin. The umbilical cord is of a brownish-red color, flattened, semi- 
transparent, and twisted. The skin around its insertion is red and 
congested. 

The head should be examined for the marks of injuries. Very 
commonly some portion of the scalp will be found swollen and infil- 
trated with blood and serum. This may be the caput succedaneum 
formed during delivery. The mouth and nose should be examined 
for the presence of any foreign bodies which might have caused suf- 
focation. 

The neck should be examined for marks of strangulation. The 
umbilical cord may be twisted around the child's neck and strangle 
it. The mark left by the cord is usually continuous, broad, not ex- 
coriated, sometimes accompanied by ecchymoses in the skin. 

The entire body should be examined for the presence of vernix 
caseosa, blood, marks of injury, and the existence of putrefaction. 
It should be remembered that putrefaction is apt to commence ear- 
lier in the bodies of young children than in those of adults. 

The umbilical cord may be cut or torn. It usually separates by 
the fifth day, sometimes not until the tenth. If the umbilicus is cica- 
trized and healed the child has probably lived for three weeks. A 
zone of redness around the insertion of the cord may exist previous 
to birth. Redness and swelling (which may disappear after death) 
with suppuration can only be found in a child which has lived for 
several days. The drying and mummification of the cord may take 
place as well in dead as in living children. It is possible for a child 
to die by hsemorrhage from a cut or torn cord, either before or after 
it has breathed. 

The extremities may exhibit fracture of the bones. These may 
occur during intra-uterine life, from injuries to the woman or from 
unknown causes.; or may be produced by violence in delivery, or by 
injuries after birth. 



46 THE METHOD OF MAKING 

INTERNAL EXAMINATION. 

The Head. — The f ontanell.es and sutures should first be examined 
as to their size and for penetrating wounds. An incision should then 
be made through the scalp across the vertex, and the flaps turned 
backward and forward as in the adult. With a small knife the 
edges of the bones should be separated from the membranous sutures 
and the dura mater, beginning low down in the frontal and going 
back into the lambdoidal suture on either side. The bones are then 
drawn outward and cut through around the skull with strong scis- 
sors. The brain is removed and examined as in the adult. 1 

Effusions of blood — cephalhematoma — may be formed, soon aftei 
birth, between the pericranium and bone, or, more rarely, between 
the dura mater and bone. Clots are also found between the dura 
mater and skull ; between the dura and pia mater ; more rarely in 
the substance of the brain, as the result of protracted or instrumental 
deliveries, or of injuries after birth. 

The cranial bones may be malformed, or exhibit the lesions oi 
rickets or caries, or be indented, fissured, or fractured. These latter 
lesions may be produced during intra-uterine life by injuries to the 
mother, by unknown causes, by difficult deliveries, or by direct vio- 
lence after birth. 

In cases of chronic internal hydrocephalus in young children, ir 
which the ventricles are much dilated and the brain substance thinned 
over the vertex, the brain is very apt to be torn in removal, and the 
amount of dilatation thus becomes difficult of determination. It is. 
therefore, better in such cases to place a pail of water beneath the 
head, or even immerse the latter in it, and remove the brain in the 
water. In this way it floats after removal, supported on all sides. 11 
may now be opened in the water and the extent of the lesion deter- 
mined at once, and parts saved for microscopical examination. 

If it be desired to preserve the brain for demonstration of the le- 
sion or for a museum specimen, it should be transferred unopened to s 
large jar containing a mixture of equal parts of alcohol and water. A 
portion of the ventricular fluid should now be removed with a syringe 
provided with a small canula, and replaced by strong alcohol. This 
may be done by puncturing the ventricles from below. The fluid in 
the jar, as well as in the ventricles, should be changed in forty-eighl 
hours and then gradually increased in strength until the organ be- 
comes hard. The brain may then be cut transversely across, when 
the degree of dilatation of the ventricles, etc., will be revealed. The 
brain, of course, shrinks considerably by this process, but the rela- 
tive proportions are approximately preserved. 

The brain is normally much softer and pinker than in the adult, 

1 Or an incision through the bones with a fine saw may be made as in the adult. 



POST-MORTEM EXAMINATIONS. 47 

the pia more delicate ; both may be much congested or anaemic with- 
out known cause. The ventricles contain very little serum. Malfor- 
mations, apoplexies, hydrocephalus, simple and tubercular inflamma- 
tory lesions, are to be looked for. 

Spinal Cord. — Extravasations of blood between the membranes 
of the cord may occur from the same causes as those in the brain. 
Spina bifida is the most frequent malformation. 

The Thorax and Abdomen. — These are opened as in the adult. 
The peritoneal cavity contains a very little clear serum. A red 
fluid may be produced by decomposition. The peritoneum is often 
the seat of intra-uterine inflammation. 

The Diaphragm. — In still-born infants its convexity reaches to 
the fourth or fifth rib. After respiration it reaches a point between 
the fourth and seventh ribs. Its position is, however, so variable 
that it is of little diagnostic importance. 

The Thorax. — The thymus gland, at this period very large, occu- 
pies the upper portion of the anterior mediastinum, covering the tra- 
chea and large vessels. Its average weight is about 15.5 gm. (| oz.). 
It is usually about 5 cm. (2 in.) long, 3.8 cm. (1| in.) wide at its 
lower part, and about .63 to .85 cm. (i to ^ in.) in thickness. It may 
be hypertrophied and compress the large vessels, or be inflamed and 
suppurating. 

The heart lies more nearly in the median line than in the adult. It 
weighs from 46 to 108 gm. (1-j- to 3 J oz.). The ventricular walls are 
of nearly equal thickness. The pericardium contains very little se- 
rum. A considerable quantity of red fluid may accumulate here as a 
result of decomposition. There may be small extravasations of blood 
beneath the pericardium in still-born children and in those born alive. 
Pericarditis with effusion of serum and fibrin, and endocarditis with 
consequent changes in the valves, may exist before birth. Malfor- 
mations and malpositions of the heart cavities and large vessels are 
not infrequent. The time of closure of the foramen ovale and the 
ductus arteriosus varies very widely in different cases. 

The pleural cavities contain very little serum, but decomposition 
may lead to the accumulation of a considerable quantity of red fluid. 
Small extravasations of blood in the subpleural tissue may be found 
in children which have died before birth and after protracted labors. 
Inflammation, with exudation of serum, fibrin, and pus, may exist 
before birth. 

The lungs in a still-born child are small, do not cover the heart, are 
situated in the upper and posterior portion of the thorax, are of a dark- 
red color and of firm, liver-like consistence, and do not crepitate. In 
a child born alive, and which has respired freely, the lungs fill the 
thoracic cavity, but do not cover the heart as much as in the adult ; 



4b THE METHOD OF MAKING 

they a/e or' a Light-red or pink color, and crepitate on pressure. It: 
spiration has been incompletely performed we find various interme 
ate conditions between the f cetal and inflated states. 

If any doubt exists as to respiration having taken place, it is ci 
tomary to employ the hydrostatic test. This is done by placing 1 
lungs, first together, then separately, and afterward cut into sm 
pieces, in water. It is commonly said that if they sink the child 1 
not breathed ; if they float it has. This test is not, however, a certe 
one. Taylor says regarding it : 

1. That the hydrostatic test can only show whether a child has 
has not breathed, not whether it was born alive or dead. 

2. That the lungs of children who have lived after birth may sii 
in water, owing to their not having received air or to their being 
a diseased condition. 

3. That a child may live for some time with the lungs only pari 
inflated. 

4. That a child may five for twenty-four hours when no part of 
lungs has been penetrated by air. 

5. The sinking of the lungs is no proof that a child has been bo 
dead. 

6. That the lungs of children which have not breathed and ha 
been born dead, may float in water from putrefaction or artificial i 
flation. 

The lesions of inflammation, and vesicular and subpleural emph 
sema, may be found in the lungs of new-born children. 

The pharynx should be opened and examined for foreign bodies 

The larynx and trachea should be examined for the lesions of i 
flammation and for injuries to the cartilages. 

The thyroid gland weighs about 12 gm. (3 3 ). It may be 
enlarged as to interfere with respiration. 

The Abdomen. — The kidneys are lobulated and proportionate 
larger than in the adult. There may be eochymoses on their surf ac 
inflammation ; deposits of uric acid and urates in the tubules of t 
pyramids ; cystic dilatation of the tubules, sometimes reaching i 
enormous size. There may be absence or retarded development 
one kidney. Malformations and malpositions of the kidneys are 
frequent occurrence. 

The suprarenal capsules are large. They may be dilated in 
large cysts filled with blood. 

The spleen is large and firm. It may be abnormally enlarge 
and its surface is sometimes covered with fresh inflammatory exud 
tions. 

The intestines. In the small intestines inflammation and swe' 
ing and pigmentation of the solitary and agminated follicles (lymf 



POST-MORTEM EXAMINATIONS. 49 

nodules) are sometimes found. The large intestine usually contains 
meconium, but this may be evacuated before or during birth. The 
sigmoid flexure is not as marked as in the adult. 

The formation of gas in the stomach and intestines does not usually 
take place until respiration is established. If decomposition has com- 
menced, however, gas may be formed as a part of the process. 

The liver is of a dark-red color, is large, and contains much blood. 
Its size diminishes after respiration is established. The size is so vari- 
able, before and after respiration, that it gives little information as to 
the age of the child. Large extravasations of blood are sometimes 
found beneath the capsule of the liver without known cause. A 
variety of pathological conditions, fatty and waxy degeneration, 
gummy tumors, etc. , may be found. 

The bladder may be full or empty, both in still-born children and 
in those which have breathed. Dilatation and hypertrophy may exist 
during intra-uterine life. 

Generative Organs. — The external generative organs in both 
males and females are more prominent than in adults. The ovaries 
are high up in the pelvis and large ; the cervix uteri is long ; the body 
small and lax, resting forward against the bladder. Phimosis in the 
male is the normal condition. Malpositions and retarded develop- 
ment of the testicles should be noticed. It should be observed 
whether the anus is perforate. 

The Bones, in suspected cases, should be examined for the 
lesions of inflammation, rickets, and syphilis. 

Preservation. — The various foetal tissues may be preserved by the same methods 
as are employed for those of the adult ; but as they are very delicate they should be 
handled with great care and the preservative fluids changed with sufficient frequency. 



GENEEAL METHODS OF PEESEEYIJ^G 

PATHOLOGICAL SPECIMENS AND PEE- 

PAEING THEM FOE STUDY. 



It is not our purpose in this section to give a complete account of 
the technical procedures required in the study of pathological speci- 
mens, since the methods are for the most part identical with those 
employed in the study of normal tissues, with which the student or 
practitioner is presumably familiar before prosecuting pathological 
studies. We wish simply to give a few brief hints as to the general 
methods which we have found most useful. Additional details will 
be found in parts of the book dealing with special tissues and organs. 

The Study of Fresh Tissues. — Although for the most part the 
conditions for the minute study of tissues are more favorable after 
they have been fixed and hardened by a suitable chemical agent, it 
is yet in many cases very important to examine them in the fresh 
state. For this purpose they may be teased apart in a one-half - 
per-cent solution of sodium chlorid and mounted and studied in the 
same. 

If the material to be studied be fluid or semi-fluid, such as exu- 
dates from mucous membranes, pus, etc., and requires dilution for 
the separation of its structural elements, a one-half of one-per-cent 
aqueous solution of sodium chlorid may be used, and in this the 
specimens may be covered and studied. Solid tissues may be teased 
apart and studied in the same solution. 

When structural elements are mingled with a large quantity of 
fluid they may be gathered for study by sedimentation, or, better, as 
a rule, by the use of one of the numerous forms of centrifugal 
machines constructed for this purpose. 

Much structural detail may be revealed in fresh tissue elements 
by allowing a drop of Carnoy's fluid to run under the cover glass 
and mingle with the salt solution, the flow being directed by a bit of 
filter paper put close to the edge of the cover glass on the side oppo- 
site to that on which the coloring fluid is added. Carnoy's fluid is 
made by adding to a saturated aqueous solution of methyl green one 



GENERAL METHODS OF PRESERVING PATHOLOGICAL SPECIMENS. 51 

per cent of acetic acid and one-tenth of one per cent of osmic acid. 
Specimens prepared in salt solution cannot usually be preserved, but 
those mounted in Cafnoy's fluid may be kept for a time by replacing 
the latter with equal parts of glycerin and one-half-per-cent. salt 
solution. 

When an immediate result Of an examination of a solid tissue is 
required, satisfactor}^ results may be -obtained by a combination of 
the freezing method for fresh tissues with the use of formalin as a 
fixative as suggested bj r Cullen. 1 Any form of freezing microtome 
and either ether or liquid carbonic acid may be used. 

Cullen's procedure is as follows: The frozen sections are put in 
a five-per-cent. watery solution of formalin (see p. 54) for from 
three to five minutes; in fifty-per-cent alcohol for three minutes; in 
absolute alcohol for one minute. They are now washed in water, 
stained with hematoxylin, decolorized in acid alcohol (one-per- 
cent hydrochloric acid), rinsed in water, contrast stained and de- 
hydrated with eosin alcohol, cleared with creosote or oil of cloves, 
arid mounted in balsam. 

For very delicate tissues, and especially when the preservation of 
the blood is desirable, Cullen recommends the placing of small pieces 
of the fresh tissues in ten-per-cent formalin for two or three hours; 
then making frozen sections, staining, and mounting as before. 

The disintegration of the sections after they thaw, and especially 
the considerable shrinkage which they undergo on treatment with 
alcohol, maj r both be largely obviated by spreading the sections as 
they thaw on an albumin fixative film upon a cover glass or slide as 
described for paraffin sections, page 59, and conducting the harden- 
ing and staining manipulations with the specimen in position upon 
the glass. 

In case the freezing apparatus is not at hand, satisfactory sections 
for early diagnosis may be obtained within twenty-four hours by the 
following procedure, suggested by Hodenpyl. 

Portions of tissue not more than 1 c.c. square and 0.3 c.c. thick 
are placed for two hours in eighty-per-cent alcohol ; then for from one 
to two hours in ninety-five-per-cent alcohol ; one-half hour in alcohol 
and ether equal parts ; and then for from four to eight hours in moder- 
ately thin celloidin. The bit of tissue is now mounted upon a block 
in the usual way in celloidin, allowing the latter to become quite firm 
by drying it in the air, before it is placed in eighty-per-cent alcohol. 
After about one-half hour in alcohol, the sections may be cut with 
the microtome and are stained and mounted in the usual way. 

Decalcifying. — Bones which are the seat of lesions and calcified 

1 Cullen, Johns Hopkins Hospital Bulletin, April, 1895. 



IH1BHHH 



52 GENERAL METHODS OF PRESERVING 

tissues in which hard and soft parts are associated must be freed 
from lime salts before thin sections can be made from them. 

Tissues which are to be decalcified should be in small pieces and 
first well hardened in alcohol or Muller's fluid. 

A variety of agents may be used for the removal of the lime. 
But the following methods will suffice for almost all purposes : 

It may be accomplished by the use of a saturated aqueous solu- 
tion of picric acid. The bone or other tissues should be cut into 
small pieces, not larger than a cubic centimetre, and suspended by a 
thread in a large quantity of the fluid, which should have an excess 
of picric acid crystals at the bottom, and should be frequently shaken. 
Considerable time is required for decalcification by this method. 

A method of rapid decalcification which gives excellent, and per- 
haps the best, results is by the combination with nitric acid of 
phloroglucin, the latter agent preventing the swelling of the tissue 
elements. One gramme of phloroglucin is dissolved with gentle heat 
in 5 c.c. of nitric acid. This solution, when effervescence has 
ceased, is of a ruby-red color. To this are added 70 c.c. of strong- 
alcohol and 30 c.c. of water. Small pieces of bone or other tissue 
are suspended by thread in relatively large quantities of this fluid. 
In from one to twenty-four hours, depending upon the size of the 
piece of bone, the decalcification is usually complete, as may be 
ascertained by passing a needle through it. Now wash the specimens 
thoroughly in running water until no acid reaction is given by litmus 
paper; put for twenty -four hours in eighty-per-cent alcohol, and then 
in strong alcohol. Bone decalcified in this way is apt to stain much 
better with hematoxylin and eosin than after the use of other decal- 
cifying agents. In all cases the decalcifying fluid should be abundant, 
exceeding the tissues in bulk at least twenty times. 

Hardening and Preservation. — Alcohol is the most common^ 
employed tissue-hardening agent for routine purposes. It is used in 
the strength of from eighty to ninety-five per cent at first, the pieces of 
tissue to be hardened not being larger than 2 or 3 c.c. There should 
be in bulk at least ten times as much alcohol as of tissue to be hard- 
ened. A little absorbent cotton may be placed in the bottle to keep 
the blocks of tissue from sticking to the bottom. After twenty-four 
hours the alcohol should be renewed. On the third day the tissue is 
transferred to ninety-seven to one hundred per cent, alcohol for com- 
pletion of the hardening, which will usually be within five or six days. 

To obtain absolute alcohol for the purposes of hardening, the ordi- 
nary strong commercial alcohol (ninety-four to ninety-seven percent) 
maybe largely dehydrated by standing in a closed bottle with at least 
one-third its bulk of pulverized cupric sulphate which has been freed 
from its water of crystallization by heating. Alcohol thus rendered 



PATHOLOGICAL SPECIMENS. 53 

approximately absolute should be filtered or carefully decanted before 
using. Commercial alcohol may be also dehydrated by shaking with 
pure quicklime and allowed to stand for some hours in closed bottles, 
then settled and decanted or filtered. 

While for many purposes other and more delicate methods of 
hardening tissues are to be recommended, for most solid tissues in 
which bacteria are to be sought for and studied, for such specimens 
as are not quite fresh and in which the process of deca} T is to be 
immediately checked, and in general for tissues in which the deter- 
mination of topographical features for diagnostic or other purposes 
is the chief end in view, alcohol is the most useful agent. 

It is very often desirable to harden a part of a specimen for topo- 
graphical purposes in alcohol, while other portions are treated with 
agents which secure a more perfect preservation of minute cell 
structure. When large specimens are to be preserved in alcohol for 
gross demonstration or for museum purposes, the alcohol ma}' be 
used in the strength of from fift} T to sixty per cent (see page 63). It 
should be always borne in mind that under the most favorable con- 
ditions the hardening of delicate tissues by alcohol involves consider- 
able change in the minute structure of cells, owing to coagulation 
and shrinkage of their albuminous constituents. 

Mi'dler's Fluid. — In many cases pathological specimens are best 
hardened first in Muller's fluid and the process completed by alcohol. 

Midler's Fluid is made by the following formula : 

Potassium Bichromate 2 parts. 

" Sulphate 1 part. 

Water 100 parts. 

Most tissues are hardened in Midler's fluid with much less shrink- 
age of their delicate constituents than is the case with alcohol. For the 
use of certain staining methods, especially of nerve tissue, a prelimi- 
nary hardening in Muller's fluid is indispensable. It should, how- 
ever, be remembered that while Muller's fluid is a good hardening 
agent for nerve fibres, for ganglion cells it is very unsatisfactory. 

The specimens for Muller's fluid hardening should be cut into 
small pieces, not more than 1 or 2 cm. square, and placed in a large 
quantity of the fluid, at least ten times the bulk of the specimen, 
where they remain for two or three weeks. The fluid should be 
€hanged three or four times within the first ten days, and after this 
as often as it becomes turbid or a sediment forms. After the speci- 
mens have acquired considerable consistence, or have been in the 
fluid for the proper time, they are removed from the fluid and soaked 
for from twenty-four to forty -eight hours in water, which should be 



54 GENERAL METHODS OP PRESERVING 

frequently changed. They are then placed in equal parts of alcohol 
and water for forty-eight hours, and. then in strong alcohol, by 
means of which the hardening is completed. They may be preserved 
in eighty- per-cent alcohol. 

For the special directions for hardening nerve tissues see page 19. 

Formalin, or formol, is the trade name for a forty-per-cent 
aqueous solution of formaldehyd. In dilute solutions it is a valu- 
able fixative and hardening agent for delicate tissues. It is most 
commonly used in a solution of 2 parts (of the commercial formalin) 
to 100 of water. The fresh tissues, in small pieces, are put in this 
solution for forty-eight hours, the fluid being renewed at the end of 
twenty-four hours. They are then transferred to sixty-per-cent 
alcohol for twenty-four hours, and the hardening is completed with 
strong alcohol. 

Formalin in two-per-cent solution is also useful in the preserva- 
tion of larger masses of tissue for demonstration or museum purposes. 

Osmic Acid is of great value for the hardening of small portions 
of delicate tissues, since it serves to fix the elements in a nearly 
normal condition and stains them of a brown or black color. It is 
generally used in one-per-cent aqueous solution, the tissues, in very 
small pieces and when quite fresh, being placed in it and allowed to 
remain for twenty-four hours. They are now washed in water and 
may be preserved in eighty-per-cent alcohol. 

Instead of using the one-per-cent osmic acid pure, very good 
results are obtained by diluting it with an equal volume each of 
water and strong alcohol. This is in many cases preferable, since 
the tissues are not stained so dark by the acid, and are more readily 
preserved subsequently in alcohol. But under these conditions a 
black precipitate forms which colors the alcohol and may be found 
in the specimens. 

Flemming's Osmic Acid Mixture. — For the purpose of fixing 
delicate tissue elements to show minute structural detail, such as 
mitotic figures, this mixture is of great value. It is made of — 

One-per-cent solution of Chromic Acid .15 parts. 

Two-per-cent solution of Osmic Acid .4 " 

Glacial Acetic Acid . v 1 part. 

This mixture does not keep wbII and hence should be made up in 
small quantities. Small portions of tissue should soak in the mixture 
for twenty-four hours arid then, after thorough washing in wateiv 
are put for twenty-four hours in seventy-per-cent alcohol, then trans^ 
f erred to strong alcohol, in which they are kept. 

Osmic acid stains fat black and on this account is a valuable 
agent for the detection of this substance in the tissues. When used 



PATHOLOGICAL SPECIMENS. 55 

with this intent it is necessary to wash the superfluous solution thor- 
oughly out of the tissues with water and by repeated changes of the 
alcohol with which the hardening is completed, since otherwise a 
black precipitate may form in the tissue and lead to error. Flem- 
ming's osmic acid mixture is excellent for the demonstration of fat. 

Extremely delicate tissues or films may be fixed by direct exposure 
to the vapor of osmic acid in a closed vessel. But under these con- 
ditions the operator must be on his guard against artefacts which 
may be developed should the structural elements dry and shrivel 
before becoming fixed by the vapor. 

Corrosive Sublimate is a most excellent fixative for delicate 
structures. It does not penetrate dense tissues readily, and hence all 
pieces of tissue should, when it is used, be very small. 

A simple solution is made by saturating a one-half-per-cent. solu- 
tion of sodium chlorid with corrosive sublimate and allowing to 
cool (between seven and eight per cent of the sublimate will be 
taken up) . The excess of sublimate will deposit on cooling, and the 
solution is decanted. 

JLano^s Solution. — Mixtures of corrosive sublimate with acetic 
acid are valuable as fixatives in delicate tissues. A very useful 
form of this mixture is Lang's solution. . Its formula is : 

Mercuric Chlorid ........................... 5 gm. 

Sodium " ........................... 6 " 

Hydric Acetate. .................... 5 c.c. 

Water 100 " 

The tissues should remain in sublimate solution as a rule not longer 
than from one to three hours. 

Specimens fixed in sublimate do not stain well, and become brittle 
unless the excess of sublimate is removed. This can be largely done 
by prolonged washing in running water. But it is much more easily 
and certainly accomplished by the chemical action of dilute iodine 
solution. The specimen is removed from the sublimate mixture and 
put at once into seventy-per-cent. alcohol. To this is added from 
time to time a sufficient quantity of saturated alcoholic solution of 
iodine (or tincture of iodine) to give the alcohol a moderately deep 
iodine color. At first this color gradually disappears, and the iodine 
solution should be repeatedly added until the color persists. The 
specimens are now transferred to seventy-per-cent alcohol, and after 
twenty-four hours to strong alcohol. f 

A very excellent preservation of fragments of tissue to show 
minute cell structure, mitotic figures, etc., may be obtained by scrap- 
ing the cut surface of an organ, tumors, etc., and dropping the 
scraped-off mass into the sublimate solution. This, after from one 



56 GENERAL METHODS OF PRESERVING 

to five minutes, is decanted, the tissue fragments thoroughly and 
repeatedly washed in water and finally preserved in alcohol. These 
tiny cell clusters may now be embedded in a mass of celloidin or 
paraffin (see below), and from this sections of extreme thinness may 
be obtained. 

Although the above is the routine method of hardening tissues, 
departures from it are occasionally desirable in the preparation of 
different organs or for the accomplishmeDt of special ends. Thus, in 
some cases — as in the kidneys, for example — the preservative fluids 
are brought into more direct and immediate contact with the tissue 
elements if they are injected under low pressure directly into the 
blood vessels. Or by means of a hypodermic syringe the fluids may 
be thrown directly into the interstices of the tissue by thrusting the 
needle into them and slowly injecting the preservative agent. This 
is called interstitial injection. 

Pathological specimens which occur, or are isolated in the form 
of membranes, should be stretched with pins on a piece of wood or 
flat cork before being immersed in the preservative fluids. 

Minute structures, such as occur in exudations from the mucous 
membranes and in cyst fluids, renal casts, etc., may be hardened by 
the osmic acid mixture, by Muller's fluid, or by formalin (two 
per cent) followed by alcohol. Under these conditions renewals or 
changes of the fluids maj r be effected in tubes by the use of the cen- 
trifugal machine. The specimens may finally be preserved in 
eighty-per-cent alcohol or in glycerin to which one-per-cent formic 
acid has been added to prevent the growth of moulds. 

Embedding and Section Cutting. — Some dense tissues, after 
being well hardened, are sufficiently solid to permit of thin sections 
being made from them without further preparation, but in most 
cases very thin sections cannot be prepared without filling the inter- 
stices of the tissue with some embedding material, which gives it 
greater consistence and holds the tissue elements firmly in their 
natural relations, to one another while the section is being made. 
Celloidin and paraffin are the most generally useful materials for this 
purpose. 

Celloidin, a non-explosive, purified form of gun-cotton used in 
photography, is best obtained in the form of thin shavings, since it 
is most easily dissolved in this form. A strong solution is made in 
equal parts of sulphuric. ether and alcohol. The solution should have 
the consistence of thick molasses. The specimen, having been 
soaked for twenty-four hours in a mixture of equal parts of alcohol 
and. ether, is placed in the celloidin solution, where it remains until 
permeated by it. This will ordinarily occur, if the specimen be of 
moderate size, in from twelve to twenty-four hours. For this prelim- 



• PATHOLOGICAL SPECIMENS. 57 

inary soaking the celloidin solution may be a little thinner than 
above mentioned. If the specimen be small and require but little 
support, it may now be laid directly on the end of a small bit of 
wood and a few drops of celloidin poured around it. In most cases, 
however, it is better to make a small paper box, in which the speci- 
men is placed in a proper position and the celloidin poured in around 
it so as to completely enclose it. In either case a considerable quan- 
tity of celloidin should be poured around the specimen, since the cel- 
loidin shrinks considerably in hardening. If sections are to be cut 
with the microtome the paper box should be made by winding a strip 
of thin paper around the end of a short cylinder of wood, 1 allowing 
it to project for a sufficient distance beyond the end. The paper is 
held in place by a rubber band. We have thus a cylindrical box 
with a wooden bottom projecting below it by which the whole can be 
held in the clamp of the microtome. 

After the specimen, either free on the end of the cork or in its 
box, is surrounded by celloidin, it should be allowed to stand for a 
short time exposed to the air, so that it may harden on the out&ide 
by the evaporation of the ether. If the temperature be high the too 
rapid evaporation of the ether will cause bubbles to appear in the 
mass. This should be avoided by covering the specimen with a bell- 
jar. After the celloidin mass has acquired sufficient hardness on the 
outside to keep its shape, the whole should be floated, specimen side 
down, in seventy- or eighty-per-cent alcohol, in which the celloidin 
will harden and acquire a sufficient consistence for cutting in a few 
hours. When this is accomplished the paper may be stripped off, 
and the specimen is ready for section cutting. A little practice will 
teach the operator of what consistence to make the celloidin solution, 
how long to expose to the air, etc. 

After the sections have been cut they may be stained in the usual 
way (see below) and mounted in glycerin or balsam. If mounted in 
balsam, the oil of cloves, which is ordinarily used for clearing up the 
sections, will dissolve the celloidin. For some tissues this does no 
harm, since they are firm enough to hold together even in thin sec- 
tions ; but in handling friable and delicate tissues it is well to keep 
the celloidin in place, mounting it with the specimen, with the study 
of which it does not interfere. This may be accomplished by using 
the oil of origanum instead of oil of cloves for clearing. 

The uncut portion of tissue may be preserved, embedded in cel- 
loidin, by keeping it in eighty-per-cent alcohol. It is better, in per- 

1 The short wooden cylinders of various sizes, known as "deck plugs. " are very 
convenient for this purpose. They are cheap and may be bought of dealers io ship- 
builders' supplies. 



58 GENERAL METHODS OF PRESERVING 

manent preservation of uncut celloidin-embedded specimens in bulk, 
to cut them off from the wooden blocks, since alcohol extracts from 
these a dark resinous material which colors the specimen and inter- 
feres with the staining of sections made later. The severed speci- 
men can be readily refastened to fresh bits of wood by a drop of 
celloidin when more sections are to be made. 1 

Paraffin. — For some purposes, especially when extremely thin 
though not large sections are required, paraffin embedding is almost 
indispensable. The sections of tissues thus embedded may be cut 
exceedingly thin (2-3 mic.) and when these are fixed to the slide and 
appropriately stained the conditions for the study of cytological 
details are more favorable than by any other method. For the 
paraffin technique the specimen should be small, say \ c.c. as a 
maximum limit. The specimen is freed from the preservative fluid 
by washing in water and then is transferred to a series of graded 
alcohols as follows: thirty per cent, fifty per cent, and seventy per 
cent, and finally ninety-five per cent. The specimen remains in each 
of these alcohols for two or several hours and is then placed in abso- 
lute alcohol. Complete dehydration of the specimen in absolute 
alcohol is indispensable for the success of this method, for if the: 
slightest trace of water be left in the specimen shrinkage or other 
artificial changes in the tissues are produced, when the specimen is 
transferred to the clearing media preparatory to immersion in the 
melted paraffin. 

When the specimen is thoroughly dehydrated by absolute alcohol 
it may be transferred to xylol, remaining in this until it sinks and 
becomes clear, which takes place in an hour or two. It is then im-^ 
mersed in a small dish or glass box of melted paraffin, kept in a con- 
stant temperature bath held at 52° C, where it remains until com- 
pletely permeated by the paraffin. It is best to use paraffin which 
has a melting point of 50° C. After the specimen has remained for 
a while in the first dish of melted paraffin it is transferred to a second 
dish of the same in order to remove any traces of xylol remaining in 
the specimen, for traces of xylol are liable to make the paraffin soft 
or cohesive after the specimen is embedded. The length of time of 
the paraffin immersion depends upon the size and density of the 
specimen; as a genneral rule one-half hour is sufficient for small, soft, 
or porous fragments. An hour or one-and-a-half hours at the utmost 
is sufficient for the melted paraffin permeation. A longer period of 



1 Small squares of thick glass or small cubes of hard rubber, though somewhat 
more expensive than the "deck plugs, " are cleaner and more convenient, since the 
embedded tissue can be preserved in alcohol, fastened to the block and ready for 
cutting at any time. 



PATHOLOGICAL SPECIMENS. 59 

immersion may interfere with the finer structural details of the 
tissues. 

A small paper box considerably larger than the specimen itself 
is filled with melted paraffin, and with a warm needle or forceps the 
specimen is transferred to the paper box and set in its proper position 
in the bottom so that the surface to be cut lies against the bottom 
of the box. In order to avoid the slow cooling of the paraffin 
around the specimen in successive layers, which prevent the forma- 
tion of a homogeneous mass, the paper box with its contents is 
quickly cooled by being put into cold water, even iced water. When 
the paraffin block is hard it is fastened with paraffin on to one of the 
various disks belonging to the paraffin microtome, trimmed so as to 
have exactly a rectangular cutting surface, and sections are cut with 
a dry knife. In order to stain these sections the paraffin must be 
removed from the interstices; this may be done with xylol. But 
when the supporting paraffin is removed from the sections they are 
liable to fall to pieces during the further staining and other manipu- 
lations. The only practical plan therefore with the great majority 
of paraffin sections is to affix them to a slide and carry them in. this 
way through the various staining and mounting procedures. 

The best way of affixing delicate paraffin sections to a slide is by 
means of a thin film of "albumen fixative." This is a mixture of 
albumen and glycerin. Equal parts of white of egg and glycerin are 
thoroughly stirred together, filtered through paper, and a small 
amount of carbolic acid added to prevent the growth of micro- 
organisms. A very small drop of this albumen mixture is placed on 
one end of the slide, and with the ball of the finger or a fold of cloth 
it is spread over the rest of the slide in as thin a film as possible. 
While this scarcely perceptible film of albumen fixative is still moist, 
the paraffin sections or the ribbons of serial sections divided into 
proper lengths, are laid upon the film and gently tapped down flat 
with a small camel's-hair brush or the finger-tip. 1 

1 Not infrequently very thin paraffin sections will curl or become corrugated as 
they leave the knife, so that it is difficult to place them flat upon the fixative film. 
Should this occur, a few drops of water may be spread out in a thin layer over the 
fixative film while it is still moist on the slide, and the whole slide, with the layer 
of water upon its surface, is very gently heated over the flame— just sufficiently to 
soften but not to melt the paraffin. If the sections are then floated out on the warm 
layer of water they will uncurl and flatten out. The layer of water is then drained 
off, when the flattened sections will lie flat upon the fixative film and remain fast- 
ened there. All traces of the water are now allowed to evaporate in the air ; or, 
the evaporation of the water may be hastened by exposure to a temperature four or 
five degrees below the melting point of the paraffin. A convenient plan is to place 
such slides on top of the paraffin bath where the temperature is not sufficient to melt 
the paraffin and yet expedites the evaporation of the water. The slides must be ab- 
solutely dry before going on with subsequent procedures. -<---' 



60 GENERAL METHODS OF PRESERVING 

The slide with the attached paraffin sections is now heated over 
a flame, warmed just sufficiently to begin to melt the paraffin ; this 
is a very delicate point in the operation. Just enough heat must be 
used to melt the paraffin and no more. If tfi3 slide be heated beyond 
this point the sections may be shrunken or completely ruined. While 
the slide is still warm it is plunged into a jar of xylol, oscillated to 
and fro for a few seconds, then placed in a jar of absolute alcohol, 
then passed through a series of jars containing different strengths of 
■alcohol — say ninety-five per cent, seventy per cent, fifty per cent, and 
thirty per cent, remaining a few minutes in each, and finally into 
water. Now the sections upon the slide may be stained in whatever 
way desired, carried up through the graded alcohols to absolute 
alcohol, then cleared in xylol or other clearing media, and mounted 
in balsam. 

Tightly covered cylindrical jars or wide-mouthed bottles are used 
for the better manipulation of paraffin sections, the whole slide being 
dropped into a bottle for staining as well as for the dehydration and 
clearing. 

Section Cutting may be done in an emergency by the free hand 
with a razor ground flat on the lower side, but better sections can be 
obtained by means of a microtome, and practically all section cutting 
for microscopical purposes is done by some form of this instrument. 
One of the most useful of these is Thoma's, which is made in three 
sizes, the intermediate or the larger one being the more useful. The 
Schanze microtome is also well adapted for general work, as are some 
of the American instruments made on the same plan. For cutting 
sections of tissues embedded in paraffin, and especially for serial sec- 
tions, the Minot microtome of the improved form is excellent. 

Methods of Staining .— Sections of hardened tissues may be 
stained for microscopical study in a variety of ways, but for routine 
work the double staining with hematoxylin and eosin is most gene- 
rally useful and is applicable to nearly all cases. 

Hcematoxylin solution (Delafield's) is prepared as follows : To 
100 c.c. of saturated solution of ammonia alum add 1 gm. of hema- 
toxylin crystals dissolved in 6 c.c. of ninetj'-five-per-cent alcohol. 
This solution is exposed to the light for three or four days, the color 
meanwhile changing from a dirty red to a deep bluish-purple color. 
Then 25 c.c. each of glycerin and wood naphtha are added. This 
mixture is allowed to stand for a day or two and is then filtered, and 
the filtration is repeated at intervals until a sediment no longer forms. 

The solution is now ready for staining, and should be consider- 
ably diluted with water as it is used, the best results being obtained 
by diluting the fluid with from ten to twenty times its bulk of water. 
The sections are immersed in the fluid, and allowed to remain until 



PATHOLOGICAL SPECIMENS. 61 

they have acquired a distinct purple color which persists after rinsing 1 
in water. They are now placed for a moment in a dilute alcoholic: 
solution of eosin, and then mounted in glycerin which has heen 
colored lightly with a alcoholic solution of eosin. In this way the 
nuclei of the cells will be stained of a purple color, while the cell 
bodies, and to a certain extent the intercellular substance, will be 
colored a light rose-red. 

If specimens are to be mounted in Canada balsam, they are 
stained with hsematoxylin as before, and the eosin staining is done 
by tinging with a saturated alcoholic solution of eosin the alcohol 
with which the final dehydration of the specimen is accomplished. 
A similar result may be obtained by tinging the oil of cloves or 
origanum with which the clearing of the sections is effected. 

Gage's hsematoxylin is more dilute than the above, and chloral 
hydrate is added as a preservative in place of the wood naphtha. Its, 
formula is as follows : 

Sterilized Distilled Water 200 c.c. 

Potash or Ammonia Alum 7.5 gm. 

Chloral Hydrate 4.0 " 

Hsematoxylin crystals . . . . 0.1 " 

Add to the mixture of water and chloral hydrate the hsematoxylin 
crystals dissolved in 10 c.c. of ninety-five-per-cent alcohol. The 
proper color is developed after a few days' standing (" ripening") . 
This stain keeps rather better than Delafield's, which occasionally 
reddens and precipitates. It may be diluted for use. 

Iron Hceyyiatoxylin (Heidenhairi ] s) . — Sections are soaked for an 
hour in a two-per-cent solution of ammonia sulphate of iron, then rinsed 
with water and put for an hour in a one-half-per-cent aqueous solution 
of hsematoxylin (prepared by heating); again rinsed and put again 
in the iron solution, in which the color gradually fades. The section 
must be watched during the process of the differentiation which 
takes place in the iron solution, and when this is accomplished to a 
proper extent the section is thoroughly washed in running water and 
mounted in the usual way. This method is especially valuable for 
the study of nuclear structures, the color of these ranging from blue 
to black, depending upon the length of time of immersion in the stain 
and the grade of differentiation. 

By the use of this method micro-organisms may be stained black, 
and in this condition are, as Learning has shown, well fitted for the. 
purposes of photomicrography. 

Picro-Acid Fuchsin (Van Gieson' s). — This double stain, first 
suggested by -Van Gieson, 1 especially for the nerve tissue, has wide 
1 Van Gieson, Laboratory Notes, etc , New York Med. Jour., July 20th, 1889. 



62 GENERAL METHODS OF PRESERVING 

applications in both normal and pathological histology, and is most 
useful when following a deep hsematoxylin stain. 

It colors the fibrillated connective- tissue fibres and the neuroglia 
in general a bright or garnet red, and also the axis cylinders and 
ganglion cells. Myelin, muscle fibres, and certain other cells are 
stained yellow, while the nuclei after the hematoxylin stain are 
brownish-red in color. Van Gieson's stain is also of value, although 
its limitations in this particular are not yet fully determined, as a 
coloring agent for hyalin amyloid colloid and mucin in the tissues. 
As a differential stain for fibrillated connective-tissue fibres it is of 
value in the study of various tumors and especially of the sarcomata. 

It is commonly prepared in two strengths, the stronger for use 
especially in nerve tissue staining, the weaker for general purposes. 
The formulae and method of using as suggested by Freeborn 1 are as 
follows: 

Picro-acid Fuchsin. Stronger solution — ■ 

One-per-cent aqueous solution Acid Fuchsin. . 15 c.c. 
Saturated aqueous solution Picric Acid and 

Water each 50 " 

Weaker solution — 

One-per-cent aqueous solution Acid Fuchsin. .. 5 " 
Saturated aqueous solution Picric Acid 100 " 

The tissues may be hardened either in alcohol, Miiller's fluid, or 
formalin, but Miiller's fluid is preferable. 

Sections are first stained deeply with hsematoxylin, washed in 
water, and put into the staining fluid, in which they remain for vary- 
ing periods, depending upon the tissue and the strength of the stain, 
but in general from one to five minutes. The sections are now 
rapidly dehydrated by alcohol cleared with oil of origanum and 
mounted in balsam. 

GtolgVs Silver Stain. — While this well-known method has com- 
mended itself most highly to morphologists for special and largely 
for topographical purposes, it has not as yet taken so definite a posi- 
tion in the armamentarium of the pathologist as to bring it within 
the scope of this handbook. 

There are many methods of staining and numerous slight modi- 
fications of old and approved methods. While some of the special 
staining methods are useful in the attainment of certain ends, 
the few simple methods which have been, here described will Suffice 
for most of the routine morphological work of the pathologist. 

1 Freeborn, Transactions New York Path. Soc., 1893, p. 73. 



PATHOLOGICAL SPECIMENS. 63 

Methods of "Preserving Specimens for Gross Demonstration 
and for Museums. — When specimens of diseased tissues or organs 
are to be preserved entire for exhibition in jars in a museum, it is in 
most cases desirable first to get rid of the blood. This may be 
accomplished, as a rule, by putting them for twenty-four hours in 
running water, after they have been sufficiently opened so that the 
water can get to them. They are now brought into proper condition 
by the removal of superfluous parts and the requisite dissections. 
Then they are carefully brought into the position and form which it 
is wished to preserve by stuffing with horsehair or absorbent cotton 
and by the use of thread. When thus carefully adjusted they are 
either suspended or laid on a wad of absorbent cotton in sixty- to 
eighty-per-cent alcohol. In this they usually become hard, and are 
finally, after the removal of the temporary stuffing and braces, trans- 
ferred for permanent exhibition to fresh, clear eightj^-per-cent alcohol. 
This description applies especially to such specimens as have cavities 
to distend or display. 

The more simple specimens, such as the solid viscera, tumors, 
etc., may be freed from blood in the same way and hardened in 
sixty -per-cent alcohol. 

In many cases an excellent hardening is obtained by injecting the 
preservative fluid through the blood vessels. The lungs are well 
hardened by pouring the fluid through the trachea into the air 
spaces. 

Methods have been from time to time suggested for the preserva- 
tion of gross specimens so as to show in part at least their natural 
colors. None of these methods have proved very satisfactory. On the 
whole a recent method devised by Jores l is the most promising, 
for in many specimens the color of the blood is in a measure 
preserved. This method is summarized as follows. The fresh speci- 
mens arranged in proper position for display are put for twenty-four 
hours in the following solution 

Formalin 5 parts. 

Sodium Chlorid 1 part. 

Magnesium Sulphate 2 parts. 

Sodium Sulphate 2 " 

Water 100 " 

The quantity of the solution should be liberal, and if the speci- 
mens be large they may remain for two days in the solution, the 
latter being renewed at the end of the first day. 

The specimens, rinsed off with alcohol, are now put into strong 

1 See Jores, Centbl. f. alJg. Path. u. Path. Anat., February 29th, 1896. 



64 GENERAL METHODS OF PRESERVING 

alcohol (ninety-five per cent), where they remain until they are per- 
meated by the fluid (usually twenty-four to forty-eight hours). 

The color of the specimens, lost in the formalin, is partially 
restored by the alcohol. They are now placed for permanent preser- 
vation in equal parts of glycerin and water. 

Formalin (two-per-cent solution) and alcohol alone are useful for 
preserving gross specimens either for demonstration or museum pur- 
poses. The fresh specimen should be placed directly, without 
removal of blood, into an abundant quantity of the solution, which is 
renewed at the end of forty-eight hours. After three or four days 
the hardening is completed with sixty-per-cent and eighty-per-cent 
alcohol. Certain color features of gross specimens are often fairly 
well preserved in such formalin specimens. 

Firm-walled cysts of various kinds are well preserved in a natural 
condition of distention by drawing off the natural contents through 
a fine canula and refilling with and immersing in the following solu- 
tion, known as Flemming's Chromic and Acetic Acid Mixture: 

One-per-cent Chromic Acid solution 20 parts. 

" Acetic Acid solution 10 " 

Water .....:70 " 

After soaking for forty-eight hours in this mixture the tissue, as 
far as it has penetrated, becomes firm and stiff and of a greenish-gray 
color. The specimen is now washed thoroughly in running water 
and preserved in eighty-per-cent alcohol. 

Cysts, such as echinococcus cysts, small embryos in their mem- 
branes, cystic kidneys, etc., may be preserved in a nearly natural con- 
dition by placing them in a five-per-cent aqueous solution of chloral 
hydrate, and after a week replacing this by a ten-per-cent solution of 
the same, in which they may be permanently preserved. Such 
specimens may be preserved in a saturated aqueous solution of 
chloroform, or in formalin (two per cent). 

We would most urgently commend to the reader the importance 
of putting pathological specimens which are to be hardened and sub- 
sequently examined microscopically, at the earliest possible moment 
into the preservative fluids, which should always be abundant. 
And, furthermore, when specimens are large it is very desirable to- 
cut them open, so that the fluids mRy come into direct contact with 
the tissues. It should be borne in mind that immediately after death 
or the removal of parts from the body, especially in warm weather, 
changes commence in the tissues and progress very rapidly, so -that 
in some cases a few hours' or even a few moments' delay will not 
only render subsequent microscopical examinations difficult and un~ 



PATHOLOGICAL SPECIMENS. 65 

satisfactory, but may lead to serious errors. As above stated, 
M tiller's fluid, alcohol, and formalin are the most generally useful 
agents. Carbolic acid and glycerin should not be used, even for 
the temporary preservation of fresh tissue. They not only do not 
harden and preserve the tissue elements, but they — especially glycerin 
— render them almost wholly useless for microscopical examination. 

The not uncommon practice of wrapping a specimen in a cloth 
soaked in alcohol or carbolic acid, and permitting it to remain in 
this for hours or days, is of no use whatever in preserving specimens 
of which microscopical examinations are to be made. Almost 
equally useless is the too common practice of placing a specimen in 
a bottle which it nearly fills, and pouring a little preservative fluid 
around it. Not only should the proper fluid be used, but it should 
be abundant, and the specimen so prepared and arranged that it may 
come into direct contact with it. 
6 



PART II. 

CHANGES IjST THE CIRCULATION OF THE 

BLOOD. 

CHANCES IN THE COMPOSITION AND 
STRUCTURE OF THE BLOOD. 

HYPERTROPHY, HYPERPLASIA, REGEN- 
ERATION, DEGENERATION, ETC. 

INFLAMMATION. 

ANIMAL AND YEGETABLE PARASITES. 

INFECTIOUS DISEASES. 

TUMORS. 



CHANGES IS THE CIBCULATIOJST OF THE 

BLOOD. 



HYPEREMIA AND ANAEMIA. 

There is an important series of changes in the character of the 
circulation during life which may, when death ensues, either alter 
considerably in appearance or disappear altogether. Among the 
more important of these changes are hypercemia — excess of blood in 
a part ; and ancemia— deficiency of blood in a part. These condi- 
tions and the causes which lead to them will not be described in de- 
tail in this book, which has chiefly to do with alterations of the tissue 
which persist and may be studied after death. Tissues which have 
been the seat of a temporary, and sometimes of a prolonged, hyperae- 
mia, may show to the naked eye nothing abnormal after death, or 
they may look redder than normal ; they may be oedematous, and 
more blood than usual may flow from them when incised. On micro- 
scopical examination the blood vessels may be normal in appearance, 
or more or less distended with blood. Long-continued hyperaemia 
may lead to haemorrhage and transudation, to pigmentation, to 
hyperplasia of tissue, or to an atrophy of tissue through pressure, or 
even to death of tissue. 

The paleness which is characteristic of ancemic tissues may not 
be evident after death. Anaemia may lead to no recognizable micro- 
scopical changes. On the other hand, if long continued it may in- 
duce atrophy and fatty degeneration, and, if excessive, may lead to 
death of tissue. 

HEMORRHAGE AND TRANSUDATION. 

Hcemorrhage is an escape of blood from the heart or vessels. It 
may occur from a rupture of the walls of the vessels, and is then 
called haemorrhage by rhexis. The rupture may be occasioned by 
injury, by some disease of the walls of the vessels which renders them 
too weak to resist the blood pressure from within, or it may occur 
from the blood pressure in the thin and incompletely developed walls 
of new-formed vessels in granulation tissue, tumors, etc. 



70 CHANGES IN THE 

Under other conditions, without recognizable changes in the walls 
of the vessels, all the elements of the blood may become extra vasated 
by passing, without rupture, through the walls of the vessels. This is 
called haemorrhage by diapedesis. These haemorrhages are usually 
small, but may be very extensive. They usually occur in the smaller 
veins and capillaries, the cells and fluids of the blood passing out 
through the cement substance between the endothelial cells. Al- 
though no marked morphological changes have as yet been detected 
which explain this extravasation, it is probable that some change in 
the nutrition of the walls does occur which renders them more perme- 
able. Haemorrhage by diapedesis is apt to occur as a result of venous 
congestion, or when the now of blood in the smaller vessels has been 
suspended for some time ; or it may result from the action of some 
poison, or from an injury not leading to rupture ; or it may occur in 
incompletely developed blood vessels, in tumors and other new-formed 
tissues. 

In the extravasation of blood by diapedesis the white blood cells 
may pass through the walls of the vessels, partly at least in virtue of 
their amoeboid movements ; the red cells, on the other hand, having 
no power of spontaneous movement, are, according to Arnold, car- 
ried passively through the walls by minute currents of fluid which, 
under the changed condition, stream in increased force and volume 
through the endothelial cement substance into the lymph spaces 
outside. 

The altered condition of the blood vessels leading to haemorrhage 
may be local or general, and in the latter case it may either be con- 
genital, as in some cases of the haemorrhagic diathesis, or it may be 
the result of some general disease, as scurvy, purpura, etc. The 
presence of bacteria in the vessels, as in malignant endocarditis and 
in haemophilia neonatorum, is believed in some cases to produce 
changes in the walls of the vessels, leading to extravasation. 

Yery small haemorrhages are called petechial ; larger, diffuse ac- 
cumulations of blood in the interstices of the tissues are commonly 
called ecchymoses or sugg illations. A complete infiltration of a cir- 
cumscribed portion of tissue with blood is called a hcemorrhagic in- 
farction. A collection of blood in a tumor-like mass is called a 
hosmatoma. Sometimes the elements of the tissue into which the 
blood escapes are simply crowded apart ; sometimes, as in the brain, 
they are broken down. 

The extravasated blood in the tissues usually soon coagulates,, 
although exceptionally it remains fluid for a long time. A certain 
number of the white blood cells may wander into adjacent lymph ves- 
sels, or they may remain entangled with the red cells in the meshes 
of the fibrin. The fluid is usually soon absorbed ; the fibrin and a 



CIRCULATION OF THE BLOOD. 71 

portion of the white blood cells disintegrate and are absorbed. The 
red blood cells soon give up their haemoglobin, which decomposes 
and may be carried away or be deposited either in cells or in the 
intercellular substance at or near the seat of the haemorrhage, 
either in the form of yellow or brown granules or as crystals of 
haematoidin. Sometimes all trace of extravasations of blood in the 
tissues disappears, but frequently their seat is indicated for a long 
time by a greater or less amount of pigment or by new-formed con- 
nective tissue. Occasionally the blood mass, in a more or less degen- 
erated condition, becomes encapsulated by connective tissue, forming 
a cyst. 

The action of phagocytes in the disposal of dead material is here, 
as it is under a great variety of conditions, an important factor in the 
restoration of the body after lesion to its normal conditions. 

Transudation is the passage, through the walls of the blood 
vessels into the lymph spaces outside, of fluid from the blood, with 
little or no admixture of its cellular elements. This occurs con- 
stantly, to a certain extent, under normal conditions, and forms the 
commencement of the lymph circulation. But when the amount of 
fluid passing through the walls of the blood vessels is increased, or 
its outflow into the larger lymph trunks is hindered so that it accu- 
mulates in undue quantity in the interstices and lymph channels of 
the tissues, the condition is pathological and is called transudation. 
An accumulation of transuded fluid in the interstices of the tissues is 
called oedema; in the serous cavities, dropsy. 

Its occurrence may depend upon some hindrance to the venous 
circulation, upon some mechanical alteration in the walls of the blood 
vessels induced by changes in the nutrient efficiency of the blood, or 
in other ways. There is furthermore strong and increasing evidence 
that the endothelial cells of the capillaries possess active secretory or 
other functional capacities which should be taken account of in the 
attempt to comprehend this as well as many other pathological phe- 
nomena and lesions. 1 

A simple interference with the outflow of lymph does not usually 
alone suffice to induce transudation, although it may favor its occur- 
rence. The transuded fluid, called transudation or transudate, 
is usually transparent and colorless or yellowish; it contains the 
same salts as the blood plasma, but less albumen. It may contain 
fat, mucin, urea, biliary acids, coloring matter of the bile ; fibrinogen 
is usually present in variable quantity, and rarely fibrin. It may 
contain endothelial cells from the lymph spaces, and a variable 
number of red and white blood cells. The amount of fluid which 

1 Consult Hamburger, Ziegler's Beitrage zur path. Anat., Bd. 14, p. 443. 



72 CHANGES IN THE 

may accumulate in the tissues varies greatly, depending upon 
whether they are loose or dense in texture. The fibres and cells 
of loose tissues may be crowded widely apart; the cells are apt to 
be more granular than normal and may be atrophied. Transudations 
occurring in inflammation usually contain a considerable number of 
white blood cells and more or less fibrin, and differ in this from the 
non-inflammatory transudations; but there is no sharp distinction 
in some cases between them. The inflammatory transudations are 
often called exudations or exudates. 



THROMBOSIS AND EMBOLISM. 

Thrombosis.— Thrombosis is a coagulation of blood in the heart or 
vessels during life. The coagulum is called a thrombus. Thrombi 
may lie against the wall of a vessel, only partially filling the lumen, 
and are then called parietal thrombi ; or they may entirely fill the 
vessel, and are then called obliterating thrombi. 

Thrombi may occur as the result of an injury to the wall of a ves- 
sel, or may follow its compression or dilatation ; they may result from 
some alteration of the wall of the vessel by disease or by the retarda- 
tion of the circulation. So long as the endothelial linings of the ves- 
sels are intact, simple retardation of the circulation does not usually 
alone suffice to induce coagulation ; but changes in the endothelium 
from a great variety of causes, such as inflammation, degeneration, 
atheroma, calcification, and the presence of tumors and foreign bod- 
ies, favor its occurrence. 

Thrombi may be composed of fibrin and of red and white blood 
cells, intermingled in about the same proportion as in an ordinary ex- 
tra vascular blood clot. These are called red thrombi, and usually 
occur from some sudden stoppage of the circulation. Other thrombi, 
usually such as form while the blood is in motion, may consist almost 
entirely of white blood cells with a little fibrin, or of these intermin- 
gled with blood plates, or they may consist almost entirely of blood 
plates ; all of these forms are called white thrombi. Red thrombi, 
when decolorized by changes in the blood pigment, may somewhat 
resemble genuine white thrombi. Mixed thrombi are usually lamel- 
lated and contain varying proportions of fibrin and red and white 
blood cells. 1 

The changes which occur in the thrombus after its formation may 
be either in the direction of degeneration or organization. In some 
cases it seems to undergo a simple shrinkage and decolorization. 

1 The character and significance of the so-called " hyalin thrombi, " -which are 
seen in the smaller blood vessels under a variety of conditions, are not yet entirely 
clear. 



CIRCULATION OF THE BLOOD. 73 

The leucocytes, the fibrin, and the blood plates may degenerate, 
forming a granular material which may become infiltrated with salts 
of lime, forming the so-called phleboliths, or vein stones ; in other 
cases the thrombi may soften and disintegrate. Certain thrombi 
contain bacteria or other infectious material, and on softening of the 
thrombus these may be carried into the circulation, producing very 
disastrous results. Finally, the thrombus may be replaced by a new 
formation of vascular connective tissue, itself disappearing as the 
new tissue is formed. This is called organization of the thrombus, 
but in reality the new connective tissue is produced, in large measure 
at least, not from the cells of the thrombus itself, but from the cells 
of the walls of the affected vessel, from whose vasa vasorum the 
new blood vessels of the thrombus also arise (compare page 124). In 
this way the vessel may be completely and permanently occluded, 
or, more rarely, a channel may be re-established through the new 
connective- tissue mass. 

Thrombi in veins may lead to hyperemia and oedema ; in arteries, 
to an ansemia whose significance will vary greatly, depending upon 
the situation of the occluded vessel. 1 

Embolism. — This is the stoppage of a blood vessel by the arrest 
in its lumen of some material carried along in the circulating blood. 
The mass causing the stoppage is called an embolus. This may 
he composed of a great variety of substances. The most common 
emboli are detached portions of thrombi, and these may have all the 
variety of structure which thrombi present. Masses of bacteria or 
other parasites, fragments of the heart valves and of tumors, droplets 
of fat from the medulla of fractured bones, parenchyma cells, 2 masses 
of pigment, bubbles of air, etc., may form emboli. Embolism is, in 
a majority of cases, confined to the arteries and to the branches of the 
portal vein. 

The primary effect of the stoppage of an arterial trunk is, of 
course, to largely deprive the region of the body to which its branches 
are distributed of its normal supply of blood. If the branches of the 
occluded artery form anastomoses with other arteries beyond the 
point of stoppage, a collateral circulation may be established and the 

Consult BeneJce, "Die Ursachen der Thrombusorganization, " Ziegler's Beitr. 
zur path. Anat., etc., Bd. vii., p. 158, 1889. 

2 The presence of liver-cell emboli in the lung capillaries and in heart clots after 
traumatic rupture of the liver and in infectious diseases involving local necroses of 
the liver has been described by various observers. Emboli believed to be composed 
largely of placental cells or of cells from the bone marrow are also described under 
various conditions. The facts relating to this subject of parenchyma-cell emboli 
and its alleged significance may be found summarized by Lubarsdi, Fortschritte der 
Medizin, Bd. xi., Nos. 20 and 21, 1893; and by Aschoff, Virchow's Archiv, Bd. 
134, p. 11. 



74 CHANGES IN THE 

embolus do no harm. If, however, the occluded vessel be a so-called 
terminal artery — that is, one whose branches do not form anasto- 
moses with other arteries — the result of the embolism is quite dif- 
ferent. When a terminal artery is occluded by an embolus the tissue 
of the affected region usually dies, and there may be an extravasa- 
tion of blood by diapedesis, leading to the formation of a dark-red, 
solidified area, called a hcemorrhagic infarction. 1 The area of in- 
farction corresponds to the region supplied with blood by the occluded 
vessel, and is usually more or less wedge-shaped. 

After a time the infarction becomes decolorized, inflammatory 
changes may occur in its periphery, the blood and involved tissues 
may undergo degeneration and be absorbed, and finally the seat of 
the infarction may be indicated only by a mass of cicatricial tissue, 
which frequently contains more or less pigment. 

In another class of cases, instead of an extravasation of blood in 
the affected region, the tissue is simply deprived of nourishment and 
undergoes necrosis. The affected area is then usually light in color 
and is called a white infarction. Inflammatory changes may occur 
in its periphery and a new connective-tissue capsule form around it, 
and the dead mass may thus persist for some time, or be gradually 
absorbed and replaced by cicatricial tissue. The scope of this book 
does not permit us to consider the somewhat complicated and often 
obscure reasons why in one case we have haemorrhagic, in another 
white infarction, as a result of embolus. 

If the embolic material consists of or contains infectious sub- 
stances, such as some forms of bacteria, in addition to the mechani- 
cal effects of simple emboli we may have gangrene, suppuration, and 
formation of abscesses, etc. , as the result of the local action of the 
infectious material, even though this may be present in very small 
amount. 

The organs in which embolic infarctions most frequently occur 
are the spleen, kidney, brain, lungs ; less frequently the retina, liver, 
and small intestines. Hsemorrhagic infarctions are not liable to oc- 

1 When an embolus lodges in a terminal artery, and the circulation in the terri- 
tory supplied by its branches ceases, the pressure from the side of the artery is re- 
duced to zero ; but, on the other hand, according to Cohnheim, the venous pressure 
now makes itself felt in a backward direction, and the capillaries and small veins in 
the affected region become crowded with blood. This blood is stagnant, however, 
and the walls of the small vessels, being deprived of their usual nourishment, un- 
dergo, it is believed, degenerative changes which favor the occurrence of extensive 
diapedesis. Thus, in the haemorrhagic infarction, not only the blood vessels but the 
extravascular tissues also are crowded with stagnant blood. The researches of 
Litten make it seem probable that, in most cases, the back pressure in the region of 
infarction comes, not from the veins, or not from them alone, but from adjacent 
arterial twigs which communicate with the capillaries of the affected region. 



CIRCULATION OF THE BLOOD. 75 

cur in the liver from emboli in the branches of the portal vein, on 
account of the blood supply which may come to the affected region 
through the branches of the hepatic artery. On the other hand, em- 
bolic abscesses from infectious emboli are of not infrequent occur- 
rence here. Hemorrhagic infarctions may occur exceptionally in re- 
gions not furnished with terminal arteries, as in the small intestines. 



CHANGES IN THE COMPOSITION" AND 
STRUCTURE OF THE BLOOD. 



The coagulability of the blood and the characters of the resulting 
clot vary widely, depending partly upon the composition of the blood 
and partly upon the conditions under which the coagulation occurs. 
There may be very little coagulation of the blood in death from the 
exclusion of air from the lungs, or from diseases and accidents which 
in any way interfere with the aeration of the blood and permit the 
accumulation of carbonic acid within it. Thus, in death from stran- 
gulation or drowning, many chronic diseases, scurvy, and under 
many conditions which we do not understand, the blood may remain 
fluid, or nearly so, after death. On the other hand, in a variety of 
acute inflammatory diseases, such as rheumatism, pneumonia, etc., 
very voluminous clots may be formed, although this is by no means 
constantly the case. The fact that large clots form after death is not 
conclusive evidence that an undue amount of fibrin-forming elements 
were present in the blood, nor does the absence of marked coagula- 
tion prove a diminution in the blood of fibrin-forming elements. 

The composition of the clot varies with the rapidity of its forma- 
tion and with the specific gravity of the plasma. Clots very rapidly 
formed in plasma of high specific gravity, or in still slowly circula- 
ting blood, are apt to be dark red, from admixture of red cells and 
fibrin. After complete failure of circulation, especially in plasma of 
low specific gravity, the red cells tend to settle to dependent vessels. 
Yellowish-white succulent clots then form in the clear supernatant 
plasma, while soft black clots result from the excess of red cells col- 
lected in the dependent vessels. 

The alkalinity of the blood varies greatly in disease, being 
reduced in severe forms of ansemia, in diabetes, and in infectious 
fevers. Diminution in the alkalinity of the blood continues during 
the course of infectious fevers, is progressive and extreme in fatal 
cases, and increases gradually with successful resistance to the infec- 
tious process. 

Anhydrosmia — the condition in which the blood contains an exces- 



CHANGES IN THE COMPOSITION AND STRUCTURE OF THE BLOOD. 77 

sive proportion of albumen, cells, and other solid elements — occurs in 
diseases associated with excessive serous discharges from the intes- 
tines. It is extreme in some cases of cholera, and has been noted in 
a lesser degree in other infectious diseases, as pneumonia and diph- 
theria. 

Hydrcemia is that condition in which the blood contains a large 
amount of water in proportion to the solid ingredients. It occurs in 
a variety of diseases of the heart, lungs, liver, and kidneys, and 
characterizes all forms of anaemia. 

Owing to the destruction of red blood cells in some forms of poi- 
soning, burning, etc., the blood plasma may contain free haemoglobin, 
by which it is discolored (hcemoglobincemia) , or it may be stained 
from the absorption of bile pigment. 

The blood may be actually increased in volume (plethora) , either 
by an increase in fluids, or in cells, or by simultaneous and propor- 
tionate increase of both fluid and cellular elements. 

Anaemia. — In general anaemia means a diminished quantity of 
blood or of red blood cells in the vessels of the whole or any part of 
the body. With one exception, — mild chlorosis, — it is invariably char- 
acterized by a reduction in number and change in form of the red 
cells (oligocythaemia), and by diminished alkalinity and coagula- 
bility. It is always associated with a reduction in specific gravity, 
haemoglobin, and in solid elements. Hydraemia and an increased 
tendency toward osmosis are equally constant features of this con- 
dition. The albumens remaining in the serum after coagulation are 
very slightly diminished in anaemia. 

Generally speaking, anaemia is produced by excessive haematoly- 
sis, or by defective haematogenesis, or by actual loss of blood, in bulk, 
(haemorrhage), or in its fluid ingredients (transudation). 

Clinically, anaemia may be secondary to haemorrhage, to exuda- 
tive processes, to prolonged innutrition, to chronic organic diseases 
of many kinds, to the action of poisons, to congenital hypoplasia of 
heart and arteries, to functional disturbances of an unknown nature 
in the blood-forming organs, and to wholly unknown causes. 
Simple atrophic changes in many tissues, hypertrophy of the red 
marrow, lymph nodes, spleen, liver, and thymus, fatty degeneration of 
the liver, kidneys, heart and blood vessels, with capillary haemor- 
rhages and transudations, are frequent accompaniments of severe 
anaemia. 1 

CHANGES IN THE RED BLOOD CELLS. 

These may be diminished in number and may undergo various 
changes in shape and size and structure. 

1 Ehrlich and Birch- Hirschf eld : "Ueber schwere ansemische Zustande, " Verhand. 
xi., Cong. Inn. Med., Wiesbaden, 1892. 



78 CHANGES IN THE COMPOSITION 

Oligocythemia is that condition of the blood in which the number 
of the red cells is reduced. This reduction in number may be tem- 
porary, as after haemorrhage, or it may be persistent, as in some 
forms of anaemia. The number of red blood cells may in extreme 
cases of anaemia be reduced to one- tenth of the normal, or even less; 
that is, from the normal number, which is between four and five 
million, there may be a reduction to half a million or less. 

A persistent diminution in the number of red cells may be effected 
either by increased destruction (hcematolysis) or by defective for- 
mation (ho3?natogenesis) of these elements, but the relation of the 
two factors in the production of the chronic anaemias is as yet im- 
perfectly determined. 

Excessive hcematolysis is observed after burns, is produced by 
many mineral poisons, as arsenic, phosphorus, and potassium chlor- 
ate, and may occur in infectious diseases through the action of bac- 
terial toxines. All stages of a peculiar destruction of red blood cells 
may readily be followed in the blood in malaria. In chronic infec- 
tious diseases, prolonged suppuration, and in the cachexia attending 
malignant new growths, destruction of red cells is probably effected, 
in part, by toxic agents circulating in the blood. In pernicious 
anaemia the condition of the blood may, with considerable certainty, 
be referred largely to a destruction of red cells by some unidentified 
toxic material in the blood. 

In the process of destruction of the red cells, especially if rapid, 
haemoglobin may be separated from the cells, dissolved in the plasma 
(haemoglobinaemia), and may then be excreted unchanged in the 
urine (haemoglobinuria). 

The gradual and more common form of destruction of red cells 
is attended with an alteration of the haemoglobin, effected chiefly in 
the liver, and with its deposit in the endothelial and glandular cells 
of various organs, especially in the liver, spleen, kidneys, bone 
marrow, and secondarily in any of the tissues. 

A part of the altered haemoglobin is to be found in the form of 
pigment granules, or as a diffuse deposit, in the cells of the above- 
named organs, where its content of iron may or may not be demons- 
trable by microchemical tests (hoemosiderin) . Another product of 
the haemoglobin, not containing iron, may be found in the same 
situations, in the forms of granules or crystals (hwmatoidin) . 
Finally, the derivatives of haemaglobin are excreted largely in the 
form of normal or pathological urinary pigment. The remaining 
fragments and stroma of the red cells are soon removed from the cir- 
culation largely by leucocytes, and partly by endothelial cells and 
giant cells, in the liver, spleen, and marrow. 

Defective hoematogenesis must be regarded as a cause of such 



AND STRUCTURE OF THE BLOOD. 79 

anaemias as are associated with pathological changes in the bone 
marrow (pernicious anaemia), and in the lymph nodes, spleen, and 
liver (leukaemia). This too is probably the chief cause of the 
anaemia following prolonged innutrition (secondary anaemia). The 
pathological changes in the blood-producing organs may sometimes 
arise as primary diseases of these organs, or similar changes may be 
secondary to excessive demands for the regeneration of the blood. In 
mild grades of anaemia the regeneration of the blood is attended with 
an hyperplasia of the red marrow [containing nucleated red cells of 
normal size (normoblasts)], which replaces the yellow marrow of the 
long bones. The chief defect in the production of red cells may then 
be a deficiency in haemoglobin (chlorosis). In severe and prolonged 
anaemia, under the influence of toxic agents in the blood, the repro- 
duction of cells may be insufficient, and these new cells may be more 
susceptible to the action of the toxic agent, which is itself the cause of 
their structural defects. A "circulus vitiosus" is thus established, 
the normal development of red cells fails and is in part replaced by 
an abnormal type of blood formation closely resembling the embry- 
onal type. In such cases the normoblasts of the marrow are replaced 
by very large nucleated red cells (megaloblasts) ; from these are 
developed very large red cells which are comparatively incapable of 
the functions of the normal cell. In this way may be established a 
secondary anaemia which steadily progresses and becomes a self- 
perpetuating disease entirely disproportionate to the original cause 
(secondary pernicious anaemia) . 

As a combined result of defective haematogenesis and increased 
haematolysis, there may be found in the blood a variety of patho- 
logical and degenerative forms of red cells. 

In mild forms of anaemia, the red cells are deficient in haemo- 
globin, the blood may be pale or watery in appearance, and the cells 
appear in the fresh condition as very pale disks or as slightly refrac- 
tive rings enclosing a nearly colorless central mass. In dry prep- 
arations stained with eosin, such cells may show only a narrow red 
ring surrounding a central portion which is entirely devoid of haemo- 
globin. In this grade of anaemia there may be noted moderate 
differences in size and irregularities in shape of the red cells. In 
severe anaemia, under a variety of conditions, as after certain forms of 
poisoning, extensive burns, etc., varying numbers of very small red 
cells are seen, called microcytes. They are spheroidal or irregular 
in shape, may be excessively minute, and their haemoglobin is either 
increased, normal, or diminished. They are produced by direct 
separation of a portion of the protoplasm of other red cells. Under 
similar conditions, a variety of bizarre forms of red cells are found, 
called poikilocytes. In very severe anaemia very large red cells 



. EXPLANATION OF PLATE. 

Fig. 1. Normal Blood.— Ehrlich's triacid stain. The red cells are of nearly 
uniform size and shape. There is an abundance of haemoglobin which is evenly 
distributed, but less densely at the centre of the cells, except in those cells which 
have been very rapidly dried, when the central lighter area does not appear. On 
the left is a lymphocyte without visible protoplasm. Above and below are two mono- 
nuclear cells showing varieties in the staining quality of the nucleus. In the centre 
is a large mononuclear or transitional leucocyte. The fine neutrophile granules and 
the large eosinophil granules are nearly identical in color and are to be distinguished, 
with this stain, only by difference in size. 

Fig. 2. Chlorosis.— M. M., female, 28 years. Red cells, 3,400,000. Hb., 
thirty-five per cent. Eosin and methylen blue. The red cells are moderately re- 
duced in number and there are moderate variations in their size and shape. They 
show a uniform and nearly invariable diminution in haemoglobin. In the upper 
left quadrant is a cell showing a gathering of haemoglobin into a dense central mass. 
In a cell on the left is represented the appearance in the central portion of a mass 
devoid of haemoglobin and staining lightly with methylen blue. Such degenera- 
tive changes are common in anaemic blood and are not to be confounded with nu- 
cleated red cells, normoblasts, one of which is shown in the upper right quadrant. 
The polynuclear and large mononuclear leucocytes are intended to represent the 
mixed leucocytosis of this condition. Above are a few blood plates. 

Fig. 3. Primary Progressive Pernicious Anaemia. — O. H. , 44 years. Red 
cells, 675, 000. Hb. , fifteen per cent. Eosin and methylen blue. The red cells are very 
much reduced in number, and do not form rouleaux. There are extreme variations 
in size, shape, and quantity of haemoglobin. The large nucleated red cells, megalo- 
blasts and gigantoblasts, were rather numerous. The upper one shows a small nucleus 
in the resting stage, the lower one a nucleus in early mitosis. The megalocyte in the 
centre shows an excess of haemoglobin, the one at the base of the field is deficient in 
haemoglobin and its outline is imperfect. In this case the eosinophile cells and the 
mononuclear leucocytes were increased in number. 

Fig. 4. Secondary Pernicious Anaemia. — C. N., 29 years. Chronic malaria. 
Red cells, 1,900,000. Hb., twenty -five per cent. Triacid stain. The red cells show 
extreme differences in size, shape, and content of haemoglobin. Most of the cells are 
deficient in haemoglobin. Nucleated red cells were not seen. The leucocytes, es- 
pecially the polynuclear forms, were increased in number, and a few myelocytes were 
present, one of which is shown on the right. 

Fig. 5. Lieno-lymphatic Leukaemia. — Eosin and methylen blue. The red 
cells are much reduced in number but do not show great differences in size, shape, 
or content of haemoglobin. No nucleated red cells were found. The increased 
number of leucocytes consisted principally of small and large mononuclear cells. 
On the left is seen a basket-shaped nucleus without demonstrable cell body. 

Fig. 6. Myelogenous Leukaemia (Nearly Typical) . —Triacid stain. The 
red cells are much reduced in number, show moderate differences in size and shape, 
but usually contain an abundance of haemoglobin. A few normoblasts were seen. 
The increased number of leucocytes consists largely of myelocytes and polynuclear 
leucocytes. In the centre is a large myelocyte with very pale eccentric nucleus 
(CorniVs myelocyte) . Above are myelocytes of ordinary size and with more deeply 
staining nuclei (Ehrlich's myelocyte) . On the left is a large eosinophile myelocyte. 
On the right is a smaller cell with some very large granules, staining very dark red, 
and showing many of the characters of the " mast cell. " 



CHANGES IN THE COMPOSITION AND STRUCTURE OF THE BLOOD. 81 

occur in considerable numbers. These cells, called megalocytes, are 
derived from the large nucleated red cells of the marrow, and their 
appearance in the blood indicates the early onset or actual establish- 
ment of some form of progressive anaemia (see Plate, Fig. 3). 

Amoeboid movement of megalocytes has been observed in speci- 
mens examined on a warm stage from the blood of pernicious anaemia 
and malaria. The tendency of the red cells to form rouleaux is 
much diminished or absent in very grave anaemia. 

In addition to the loss of haemoglobin, as observed in most cells in 
chlorosis, the megalocytes may show an altered reaction to eosin, 
staining brownish-red with this dye instead of the usual light- red. 
This abnormality has been referred to a change of haemoglobin to 
methaemoglobin (Ehrlich). In malarial blood, red cells frequently 
show an altered reaction to eosin and other dyes, indicating an al- 
tered form of haemoglobin. 

Not infrequently a loss of haemoglobin is associated with a change 
in the stroma of the cell, so that the central mass stains slightly with 
methyl blue. To this change the name of anaemic degeneration has 
been given (Ehrlich). Instead of a uniform loss of haemoglobin this 
constituent of the cell may be condensed in the form of small gran- 
ules occupying the centre of the cell body and staining more deeply 
with eosin than do normal cells (Plate, Fig. 2) . 

It should be remembered that during the manipulations required 
in making dried specimens the red cells may suffer a variety of arti- 
ficial changes, many of which are very confusing. 

Nucleated Red Blood Cells are found in the blood in all forms of 
anaemia, and their appearance indicates regenerative activity on the 
part of the blood-producing organs. Their presence in the blood, 
though at all periods of extra-uterine life abnormal, may usually be 
regarded as of favorable import in disease. Within a few hours after 
severe haemorrhage nucleated red cells may be noted in considerable 
numbers. During the regeneration of the blood in chlorosis, the 
occurrence of nucleated red cells is nearly constant, but subject to 
rather sudden periodical variations sometimes called "blood crises." 
In favorable cases of anaemia nucleated red cells of normal size only 
(normoblasts) (Plate, Fig. 2) are to be seen, whose compact, darkly 
staining nucleus may be found either in the centre of the cell or 
slightly protruding from the periphery, or apparently quite extruded 
from the cell and free in the plasma. 

In severe anaemia attended with an abnormal type of blood for- 
mation, very large nucleated red cells (megaloblasts) (Plate, Fig. 3) 
appear in varying numbers. The protoplasm of these cells often shows 
an excess of haemoglobin, but frequently the reddish-brown stain pro- 
duced by eosin indicates an altered form of haemoglobin, or rarelv 
7 & 



82 CHANGES IN THE COMPOSITION 

very fine basophile granules may be demonstrated by treatment with 
methyl blue. The nuclei of the megaloblasts may be single and 
compact, or a single large nucleus may show stages of direct division, 
or in extremely large cells (gigantoblasts) (Plate, Fig. 3), the nuclei 
may present phases of normal or pathological mitosis. 

CHANGES IN THE WHITE BLOOD CELLS. 

The leucocytes of normal blood may be classified according to 
their place of origin, or by the character of their nuclei, or by the 
reaction of the granules in their protoplasm to certain dyes. The 
most serviceable classification is that based both upon the character of 
the nucleus and upon the reaction of the protoplasm to dyes, accord- 
ing to which we may distinguish in normal blood the following 
forms (see Plate, Fig. 1) : 

1. Lymphocytes, small leucocytes of about the size of red cells or 
larger, with a single compact, deeply staining nucleus, surrounded 
by a thin rim of homogeneous protoplasm. Large and small lympho- 
cytes may be distinguished. 

2. Large Mononuclear Leucocytes, with a single, compact or 
vesicular, rather faintly staining nucleus and a relatively large 
amount of protoplasm, in which fine basophile granules may some- 
times be demonstrated by treatment with basic dyes such as methyl 
blue. 

3. Transitional Leucocytes, of the same size as many of the 
large mononuclear leucocytes, with a compact or vesicular, irregular 
or incurved nucleus, and a considerable mass of protoplasm, in which 
fine basophile granules can usually be demonstrated by methyl blue. 
See page 88. 

4. Polynuclear Neutrophile Leucocytes, of the same size as the 
transitional leucocytes, with a partially or completely divided nu- 
cleus, of which the separate portions are either compact or vesicular, 
deeply or faintly staining, and with considerable protoplasm in 
which distinct granules may be demonstrated by the neutral dyes. 

5. Eosinophile Cells, of the same characters as the ordinary 
polynuclear leucocytes, but containing in their bodies large refractive 
granules which stain deeply with so-called acid dyes such as eosin. 

These various forms of leucocytes occur in normal blood, with 
slight variation, in the following proportions : 

Polynuclear neutrophile leucocytes 64 per cent. 

Large mononuclear 28 

Lymphocytes 6 

Transitional leucocytes. . , 1 

Eosinophile " 1 



AND STRUCTURE OF THE BLOOD. 83 

The numbers and proportions of the polynuclear leucocytes are in 
disease subject to very wide variations, and some abnormal forms 
of colorless cells make their appearance in the blood. 

Leucocytosis is that condition of the blood in which the leuco- 
cytes are temporarily or persistently increased in number. When 
several forms of leucocytes are increased in number and the usual pro- 
portions are but partially disturbed, we speak of mixed leucocytosis. 
Such a condition is seen in some forms of anaemia. When the poly- 
nuclear neutrophile leucocytes alone are increased the condition is 
termed polynuclear leucocytosis, or simply leucocytosis. If the 
mononuclear cells are chiefly affected, the condition may be denoted 
as lymphocytosis. The eosinophile cells alone may be increased. 

Polynuclear Leucocytosis may be either physiological or patho- 
logical. 

Physiological Polynuclear Leucocytosis is seen during normal 
digestion, in the latter months of pregnancy, and in the first days of 
infancy, and is usually of moderate grade. 

Pathological Polynuclear Leucocytosis is produced by many in- 
flammatory and infectious diseases, and accompanies the various 
cachexias. Of the infections diseases attended with leucocytosis may 
be mentioned pneumonia, diphtheria, scarlet fever, erysipelas, rheu- 
matism, suppurative cerebro-spinal meningitis, and any disease 
associated with a pronounced exud'ative or suppurative lesion. On 
the other hand, leucocytosis is absent in uncomplicated typhoid 
fever, typhus, malaria, measles, and tuberculosis. 

The origin and significance of the leucocytosis of infectious dis- 
eases is imperfectly understood, but may be partially explained by 
the principles of chemotaxis and phagocytosis. From experimental 
evidence and clinical observation it is known that during the onset 
of some infectious diseases the entrance of bacteria or their products 
into the blood is followed by a disappearance from the circulation of 
many polynuclear leucocytes, which are removed from the larger 
vessels and lodged in the capillaries, principally in the lungs and 
liver. This condition of the blood, called hypoleucocytosis, may 
be attended with a transient reduction in temperature and weakening 
of the heart's action, and is usually succeeded shortly by the reap- 
pearance of polynuclear leucocytes in large numbers, and by a rise of 
temperature. These leucocytes are apt to gather in regions in which 
micro-organisms are abundant, and are believed to take up and de- 
stroy micro-organisms (phagocytosis), and to prevent their further 
entrance, and possibly the entrance of their products also into the 
circulation. Of the place and method of origin of these new leuco- 
cytes very little is definitely known. 

In many very severe cases of infectious disease, such as pneu- 



84 CHANGES IN THE COMPOSITION 

monia, diphtheria, and peritonitis, the initial hypoleucocytosis per- 
sists, in which event the disease usually runs an asthenic and fatal 
course, with a tendency to low temperature and feeble pulse, and 
without the customary increase of leucocytes. 

When leucocytosis is established the grade varies frequently with 
the extent of the local lesion and the height of the fever produced by 
the infectious process, and disappears with, or soon after, the decline 
of the disease. In general, according to our present knowledge, the 
leucocytosis of infectious diseases may be regarded as the effort of 
the blood-producing organs to protect the blood and tissues by means 
of leucocytes against the invasion of micro-organisms and against the 
action of toxins present in the circulation. 

The blood in typhoid fever presents a peculiar variation from that 
in most infectious diseases. In the first weeks of the disease there is 
usually a reduction in the number of leucocytes, especially of the 
polynuclear forms. In the latter weeks the lymphocytes may form 
eighty per cent of the leucocytes present in the blood. Each relapse 
is attended with an increase of the lymphocytosis, while an increase 
of polynuclear leucocytes usually occurs with complications only. 

In the various forms of tuberculosis there is no leucocytosis unless 
the lesion is markedly exudative in character, or is complicated by 
suppuration, or chronic anaemia. It is especially in pulmonary tuber- 
culosis that secondary infection with the pyogenic cocci produces 
exudative or suppurative lesions such as are apt to accompany leuco- 
cytosis. 

Cachectic Leucocytosis is a feature of altered conditions of the 
blood, such as are associated with the growth of malignant tumors, 
and with many diseases producing secondary anaemia. This increase 
of polynuclear leucocytes may serve to distinguish many forms of 
secondary from primary anaemia. The inflammation and toxaemia 
accompanying many new growths is a sufficient reason for the ap- 
pearance of cachectic leucocytosis, but under many other circum- 
stances its direct cause is less apparent. 1 

Hypoleucocytosis occurs not only in infectious diseases, when 
the polynuclear cells alone are reduced in numbers, but also from 
shock, reduction of body temperature, and exhaustion, when all 
forms of leucocytes may be diminished. It is a fairly constant fea- 
ture of primary pernicious anaemia. 2 

In mixed leucocytosis several forms of white cells are simulta- 



1 For further data concerning Leucocytosis, consult Bieder, Beitrage zur Kennt- 
niss d. Leucocytose, Leipsic, 1892. 

2 For Hypoleucocytosis, consult Lowit, " Studien iiber Physiol, de Pathol, d. 
Blutes u. d. Lymphe, " Jena. 1892. Moing, "Toxic Hypoleucocytosis, " New York 
Medical Journal, March, 1895. 



AND STRUCTURE OF THE BLOOD. 85 

neously increased in number, including the mononuclear, polynuclear, 
.and eosinophile cells, and a new form of colorless cell, not found in 
normal blood, the myelocyte, makes its appearance in the circulation. 

Myelocytes are mononuclear cells of the same size as the polynu- 
clear leucocytes, presenting a single, round nucleus, usually staining 
faintly with nuclear dyes, aud containing neutrophile granules in the 
protoplasm (Plate, Fig. 6). These cells are normally present in the 
bone marrow, and their presence in the circulation indicates increased 
activity of the blood-producing organs, especially of the bone mar- 
row. Very large myelocytes with a faint eccentric nucleus are occa- 
sionally seen in grave anaemias (Cornil's myelocyte), and eosinophile 
cells, with a single, large, faintly staining nucleus, are usually con- 
sidered as derivatives of similar cells in the bone marrow (eosinophile 
myelocytes). Mixed leucocytosis, with the presence of one or all of 
these forms of myelocytes, may accompany any of the severe primary 
anaemias, while in secondary anaemia the myelocytes may be found in 
addition to the increased number of polynuclear leucocytes. In 
leukaemia, the mononuclear cells and the myelocytes may be found in 
enormous numbers. Myelocytes usually fail to exhibit amoeboid 
movement, and their nuclei may present many phases of normal or 
pathological mitosis. 

In leukaemia a special variety of colorless cell, the "mast " cell, is 
found, often in considerable numbers, and the great rarity of its oc- 
currence under other conditions lends special diagnostic importance 
to its appearance in the blood. The mast cell is usually of about the 
same size as the large mononuclear leucocyte, with a single, rarely 
double, faintly staining nucleus occupying the larger part of the cell 
mass, and with a moderate area of protoplasm thickly studded with 
large granules which stain deeply with some basic dyes, such as 
dahlia. Mast cells are found in many tissues, usually when these 
tissues have been inflamed or subjected to prolonged disturbance of 
nutrition. Their appearance in the blood has been demonstrated al- 
most exclusively in leukaemia. (Plate, Fig. 6, shows a cell resem- 
bling the "mast cell," but this cell can be positively identified only 
by a special stain. See page 88.) 

Lymphocytosis, frequently seen in the anaemia of childhood or 
in any severe circulatory disturbance in early life, has also been 
noted in some forms of secondary anaemia (syphilis), and in an ex- 
treme degree is the chief characteristic of the blood of splenic and 
lymphatic leukaemia. 

A moderate increase of eosinophile cells has been noted under a 
great variety of circumstances, as after the crisis of pneumonia, in 
conditions of prolonged innutrition, and in splenic and myelogenous 
leukaemia, but its significance is largely undetermined. The Char- 



86 CHANGES IN THE COMPOSITION 

cot- Ley den crystals are occasionally found in the blood, usually at 
the same time with an increased number of eosinophile cells. 

Degenerative changes of the blood are usually indicated in the 
leucocytes by variations in the percentage of normal and abnormal 
varieties, rather than by alterations in the individual cells, for degen- 
erating leucocytes are usually quickly removed from the circulation. 
Staining reactions of the various granules, by which degenerative 
changes may be recognized, have not yet been devised. In leukaemia, 
pernicious anaemia, and diphtheria, a diminished reaction to nuclear 
dyes has been observed. In leukaemia, and in the severe infectious 
diseases, the leucocytes may be extremely cohesive, and it is believed 
that a large quantity of bacteria or toxins in the circulation may 
even affect a complete solution and destruction of leucocytes (leuco- 
cytolysis). Fatty degeneration of leucocytes has been demonstrated. 

Melancemia. — In this condition the blood contains larger and 
smaller irregular-shaped particles or masses of brown or black pig- 
ment. This condition is most frequently the result of intermittent 
and remittent fever, particularly the severer forms. It may be ac- 
companied by anaemia and leucocytosis. It does not occur in all 
cases of the above-named affections. It may be transient in char- 
acter. The pigment may be free, or more usually is enclosed in leu- 
cocytes. Under the same conditions pigment may be deposited in 
the liver, spleen, lymph nodes, bone marrow, and blood vessels. 
Owing to the deposit of pigment in the organs they may assume a 
gray or slate color. The pigment developed in malaria originates in 
the decomposition of the haemoglobin under the influence of the Plas- 
modium. Pigment which has been taken into the lungs from the 
air, such as coal dust, etc., may find its way into the blood either 
before or after deposition in the bronchial or other lymph nodes, 
and may be afterwards deposited in the spleen and liver. 

METHOD OF EXAMINATION OF THE BLOOD. 

The blood may be examined fresh on the warm stage without the 
addition of any fixative, simply surrounding the cover with oil or 
vaselin to prevent evaporation. For most purposes, however, the 
cells should be treated the instant the blood leaves the vessels in 
such a way as to retain their normal form. This fixation may be 
accomplished by the use of chemical agents (wet method) or by quick- 
drying on the cover glass or slide (dry method). 

Wet Method— Among the chemical fixative agents are osmic 
acid and a solution of corrosive sublimate. Osmic Acid : A drop 
or two of blood drawn from the cleansed finger-tip by a needle prick 
is allowed to fall into a cubic centimetre of from one- to two-per-cent 



AND STRUCTURE OF THE BLOOD. 87 

osmic acid. After an hour the blood cells may be transferred by a 
pipette to a solution of acetate of potash, in which they may be pre- 
served. 

Sublimate may be used in the form of Hayem's solution : 

Hayem/s Solution. 

Chloride of Sodium 1 gm. 

Sulphate " 5 " 

Corrosive sublimate 0.5 " 

Water, distilled 200 " 

The blood is received directly into this solution, in which it is 
studied. 

Dry Method. — It has been found that if the freshly drawn blood 
from a finger prick be immediately dried on a glass in a very thin 
layer, the cell forms are quite well preserved and may be exposed to 
the action of staining agents, by which many features are developed 
not easily seen by the wet method. 1 

For this purpose square cover glasses of medium size should be 
cleaned in strong nitric acid, rinsed in alcohol and ether, carefully 
dried, and kept free from dust. A drop of blood may be expressed 
by very light pressure only from the finger tip, previously cleansed 
with alcohol and ether, and for the best results the drop must be 
spheroidal and about one-sixteenth of an inch in diameter. One 
cover glass should be held in the forceps, or between the fingers if 
thoroughly dry, and its central point touched to the drop of blood. 
After contact with the blood this cover glass should be instantly laid 
upon a second glass so as to cover all but an eighth of an inch along 
one side, and as soon as the blood has spread to the edges the cover 
glasses should be quickly separated without pressure and dried in the 
air. If, instead of drying in the air, the specimens are rapidly dried 
over an alcohol flame, the fixation will be more successful, and many 
artificial changes in the red cells will be avoided. By this method 
the red and white cells, in the same proportions in which they existed 
in the drop, will be uniformly distributed over the cover glasses, and 
there is an opportunity for the formation of rouleaux. 

Another method, more successful in many hands, consists in 
touching the drop with the smooth edge of a glass slide, applying 
this edge with its adherent blood obliquely to a cover glass, and 
when the blood has spread along the edge of the slide, drawing it 
rapidly across the cover glass. 

! For further details concerning methods of blood examination, etc., consult 
Ehrlich, " Gesam. Mittheilungen, " Berlin, 1891. V. Limbeck, " Grundriss einer klin. 
Path. d. Blutes, v. Jena, 1896. 



88 CHANGES IN THE COMPOSITION 

For the permanent fixation of the cells and to prevent their solu- 
tion by strong dyes, one of three methods may be recommended, 
with preference in the order named: 

1. JEhrlich's Method. — The specimens are heated in a hot-air bath 
or on a copper plate, for from two to five minutes (or better twenty 
minutes) at a temperature of 105° to 110° C. 

2. Nikiforoff's Method. — The specimens are placed for five to ten 
minutes in equal parts of alcohol and ether. 

3. Hayem^s Method. — -The specimens are exposed for five seconds 
to the vapor of a two-per-cent solution of osmic acid in water, to ac- 
complish which they may be laid over a wide-mouthed bottle contain- 
ing this solution. 

Various staining agents are to be employed according to the ob- 
ject in view. Probably most information is gained from specimens 
stained by the triacid mixture of Ehrlich, which is thus prepared : 1 

Saturated aqueous solutions of 

Orange G 120-135 c.c. 

Acid Fuchsin 80-165 " 

Methyl Green 125 " 

To the mixture of these add 

Water 300 c.c. 

Absolute Alcohol 200 " 

Glycerin 100 " 

The specimens should be stained in this fluid for three to five min- 
utes, washed in water, dried, and mounted in balsam. 

The red cells are then found stained orange-yellow, the nuclei dark- 
green or blue, the neutrophile and eosinophile granules dark-red. 

Rather more uniform results, especially as regards the red cells 
may be obtained by the following method, which also demonstrates 
the malarial plasmodium and basophile granules, but not the neutro- 
phile granules. Place the specimens for two minutes in a saturated 
alcoholic solution of eosin, wash in water, and counterstain for five 
minutes in a saturated watery solution of methyl blue. The red cells 
and eosinophile granules then appear bright-red. The nuclei, baso- 
phile granules, and malarial plasmodium are stained blue. 

For the demonstration of mast-cell granules, the following Ehr- 
lich's dahlia solution may be used : 



1 Great care must be used in selecting these dyes. Those made by Griibler, of 
Leipsic, are reliable. A solution known as "Ehrlich 's triacid mixture" is on the 
market and is to be recommended. 



AND STRUCTURE OF THE BLOOD. 80 

Alcohol, absolute 50 c.c. 

Distilled Water 100 " 

Glacial Acetic Acid 12.5 " 

To this mixture add dahlia till a saturated solution is formed. 

Stain several hours, wash in water, decolorize in alcohol, or more 
rapidly in twenty-per-cent acetic acid, wash in water, dry, and 
mount in balsam. 1 

For the demonstration of mitotic figures Delafield's hsematoxylin 
(diluted), or Heidenhain's iron alum hsematoxylin, may be used. 

For the demonstration of fat in blood from a finger prick, cover- 
glass preparations dried in the air should be stained for twenty-four 
hours in one-per-cent aqueous solution of osmic acid. To avoid 
numerous sources of error, a control preparation should be previously 
placed in chloroform for twent} T -four hours to dissolve the fat, and 
the two specimens carried together through the osmic acid. In the 
one, black fat droplets will be seen, which should be entirely absent 
in the other. 2 

FOREIGN BODIES IN THE BLOOD. 

Various bodies which do not belong there, aside from those above 
mentioned, may find access to the vessels and mingle with the blood. 
Pus cells may get into the blood from the opening of an abscess into 
a vessel or from some inflammatory change in its walls. Desqua- 
mated endothelial cells from the vessel walls, either in a condition of 
fatty degeneration or in various stages of proliferation, may be 
mingled with the normal blood elements; also tumor cells of various 
kinds, fragments of disintegrated thrombi, portions of heart valves, 
etc. Crystals of bilirubin have been found in the blood in icterus. 

Fat, in a moderate amount, is a normal ingredient of the blood 
during digestion and in lactation. Under pathological conditions it 
may occur in larger and smaller droplets. This lipcemia occurs as a 
result of deficient oxidation, in diabetes, in drunkards, and in some 
cases of dyspnoea from various causes. The droplets are small and 
liable to escape observation. 

In many cases of injury, particularly in crushing fractures of the 
bone, the fat of the marrow finds its way into the blood, and it may 
collect in large drops in the vessels of the lungs, forming the so- 
called fat emboli ; or it may pass the lungs and form emboli in other 

1 In the application of any of these methods of staining the closest attention to 
detail is required for satisfactory results. 

2 For various other methods of staining "blood cells, and for detailed considera- 
tion of morphological changes in disease, we refer to Von Limbeck, "Klin. Patho- 
logie des Blutes, " 1896. 



90 CHANGES IN THE COMPOSITION 

parts, as the brain, kidneys, etc. Fat embolism in eclampsia is of 
occasional occurrence. 

The fat may be absorbed from the vessels, having produced little 
or no disturbance ; or in some cases it may produce serious results by 
the stoppage of a large series of vessels in the lungs, brain, or other 
parts of the body. 1 

The fat may be best seen by cutting sections of the fresh tissues 
with the freezing microtome and staining them at once for twenty- 
four hours with one-per-cent aqueous solution of osmic acid. They 
may then be mounted in glycerin. 

Air in the blood, as the result of an opening in the veins, is of 
occasional occurrence. If the amount of air be small it appears to 
be readily absorbed and does little or no harm. If, on the other 
hand, a large quantity is admitted to the veins at once, it collects in 
the right side of the heart, from which the contractions of the organ 
are unable to force it in any considerable quantity, and, the supply 
of blood being thus cut off from the lungs, death very quickly en- 
sues. It is especially from wounds of the veins of the neck and 
thorax that the accident is most apt to occur. But it may be due to 
the introduction of air into the uterine veins in intra-uterine injec- 
tion or in the removal of tumors. 2 

The occurrence of animal and vegetable parasites is considered, 
more in detail in parts of this book devoted to these organisms. It 
will suffice to mention here that the more important of the animal 
parasites of the blood are : the Filaria sanguinis hominis, the Dis- 
toma haematobium, and the embryos of trichina and echinococ- 
cus, which are of occasional and usual temporary occurrence. 

The various species of bacteria which may be found in the blood 
will be considered in parts of this book in which these organisms are 
treated in detail. 3 Parenchyma-cell emboli are considered on page 73. 

1 Consult for resume of this subject, with good bibliography, article by Park on 
"Fat Embolism," New York Medical Journal, August 16th, 1884. 

2 Consult Gouty, "Etudes exp. sur l'entree de l'air dans les veines," Paris, 1875, 
for experiments and older literature ; also later article by Couty, Arch, de PhysioL 
nor. et path., 2d ser., t. ir., p. 429, 1877; more recent consideration of the subject in 
Archiv fur klin. Medicin, Bd. xxxi., p. 441, 1882, by Jurgensen. 

3 For methods of bacterial study of blood with bibliography consult Sittmann,. 
Deutsches Archiv f. klin. Med., Bd. liii., p. 323, 1894. 



HYPERTROPHY, HYPERPLASIA, REGENE- 
RATION METAPLASIA. 



HYPERTROPHY AND HYPERPLASIA. 

Under a variety of conditions parts of the body or organs be- 
come larger than normal — hypertrophied. When we look for the 
structural changes to which hypertrophy is due, we find that it may 
be owing to a simple increase in size of the elementary structures 
of the part, cells, and other tissue elements. This is called simple 
hypertrophy. 

On the other hand, it is found in many cases that the increase in 
size of a part or organ is due not only, or not at all, to the increase in 
size of its elementary structures, but to an increase in their number. 
This increase in number of the structural elements of a tissue or 
organ is called numerical hypertrophy, or hyperplasia. 

Simple hypertrophy and hyperplasia are frequently associated. 

REGENERATION. 

The wear and tear of the body in the performance of its varied 
functions and labors, and the greater or smaller injuries to which it 
is frequently exposed, make indispensable for the maintenance of its 
integrity a more or less constant and widespread regeneration of 
tissue. 

This regeneration of injured or worn-out tissues, all new growths, 
as well as the hyperplasias above mentioned, are invariably brought 
about by proliferation or other changes in living cells. 

A new formation of cells in the body, so especially characteristic 
of this period of development, thus persists through lif e with varying 
degrees of activity. It is in the adult, however, under pathological 
conditions — in the course of inflammation in the growth of tumors — 
that those cell prolif erations occur which especially concern us here. 

Just as the cells of the adult organism are the offspring of one 
original cell, the ovum, so are all the new cells which appear in the 
body under abnormal conditions derived from some pre-existing cells 
by a division of their bodies. 



D2 HYPERTROPHY, HYPERPLASIA, 

The careful and minute study of cells during the act of division, 
"which has been recently made, has revealed many most curious phe- 
nomena and has opened a new world of observation nearer to the 
elementary expression of life than has seemed possible in earlier times. 
It will suffice for our purposes to briefly indicate some of the more 
striking features of the new cell lore. 

The earliest morphological changes in cell division are seen in 
the nucleus. 

Direct (Amitotic) Cell Division. — In. this, which although 
relatively rare appears to be the most simple mode of cell division, the 






^ra's* 






.*&. 



<w 



« 



m 



■ , 



* 






7 
Fig. 8.— Phases of Mitosis, or Indirect Cell Division. 

nucleus with its membrane becomes constricted and finally divides 
into two or more parts which become new nuclei. Hand-in-hand 
with or following this simple nuclear division the cell body divides, 
and thus two or more cells may form in the place of one. Sometimes 
the nuclear division is not followed by a division of the cell body, and 
thus multinuclear cells, or "giant cells," may be formed. Whether 
in this mode of cell division there may not be as yet unrecognized 
minute changes in the cell nucleus, ushering in the process, seems 
not to be altogether clear. 

Indirect (Mitotic) Cell Division. — In this mode of cell multipli- 
cation certain minute changes in the nucleus usher in the coarser 
process of division. The earlier changes which are to be seen in a 
cell about to divide are a thickening and rearrangement of the 



REGENERATION, METAPLASIA. 93 

chromatin forming the intranuclear network (Fig. 8; 1 and 2). 
As the chromatin fibres or filaments — called chromo soines — thicken, 
they group themselves into an irregular snarl or contorted mass, the 
nucleolus disappears, and the nuclear membrane becomes indistinct. 
(Fig. 8; 3). 

Now the chromosomes separate by longitudinal division into 
equal parts, and these arranging themselves in various, often stellar 
forms, slowly draw asunder in two or more groups (Fig. 8; ^,5, and 
6). Then the cell body shows a beginning constriction corresponding 
to the division of the chromosomes into masses (Fig. 8; 7). Finally 
a nuclear membrane develops around each of the new nuclei, their 
fibres become more slender and assume the resting arrangement, and 
the cell body completes its division by a deepening of its constriction 
(see Fig. 8; 8 and 9). There are countless variations and details in 
the minute processes of cell division which the scope of this work 
does not permit us to consider. But the facts already at hand are of 
extreme significance to the biologist and point toward large fields of 
research in pathology when the normal processes shall have been 
more clearly and exhaustively determined. 

In the mean time far-reaching conclusions based upon preliminary 
observations on asymmetrical karyokinesis in abnormal tissues should 
be accepted with reserve, since the details of the condition are not yet. 
fully studied and simple degenerative processes not sufficiently taken 
into the account. 1 

The term mitosis or karyomitosis is applied to this indirect mode 
of cell division on account of the involvement of the nuclear threads. 
It is also sometimes designated as karyokinesis, from the form 
changes which these threads undergo. Aside from its intrinsic bio- 
logical interest, a knowledge of mitosis in proliferating cells is of 
importance in pathology, because the recognition of mitotic figures 
often enables us to decide with certainty what particular cells or cell 
groups are involved in the formation of new tissue. 

The most significant feature, however, of the whole process of 
mitosis, with all its intricate variations, appears to be that the chromo- 
somes, during their separation into two or more clusters to form the 
basis of new cells, undergo an exact longitudinal division, so that 
under normal conditions all of the new nuclei share alike in the 
chromatin substance of the parent cell. This fact appears to be of ex- 
treme importance in the recognition of a physical basis of inheri- 
tance. 2 

1 Hansemann, Virchow's Arcbiv, Bd. cxxix. Lustig and Galeotti, Ziegler'a. 
Beitrage zur path.' Acat., Bd. xiv., pp. 225 and 249. 

2 Consult Wilson, "The Cell in Development, and in Heredity, " 1896. 



94 HYPERTROPHY, HYPERPLASIA, 

It is not necessary for us to follow in detail here the processes of 
regeneration and repair in the different tissues and organs. It should 
be borne in mind that individual cells may, even after having under- 
gone marked structural changes — as, for example, in acute granular 
degeneration — be restored to a perfectly normal condition. 

After injury or loss a full and complete regeneration of cells and 
tissues can occur only as the result of a proliferation of cells of the 
same type as those to be restored. Thus a regeneration of epithelium 
occurs by proliferation and growth of epithelial cells alone ; regene- 
ration of muscle by muscle cells ; of nerve by nerve cells, etc. In 
fact, however, in the higher types of tissue, after considerable injuries 
with loss of substance or after destructive pathological processes, 
complete regeneration is not common. This is because the highly 
specialized cells of the body are limited in their capacity for repro- 
duction closely to the domain of physiological regeneration. 

What we ordinarily call healing, in extensive wounds of the more 
highly specialized tissues, is usually a provisional makeshift repair by 
means of new-formed connective tissue. Such regeneration as takes 
place in peripheral nerves after partial destruction is brought about 
by the action of constituents of the nerve fibres themselves. But it 
is a fibrous or neuroglia-tissue healing only which is possible when 
the loss is central or extensive, and it is this alone which, after large 
injuries to the brain, achieves a patchwork repair. 

In injuries of muscle, too, the remains of muscle protoplasm may 
undergo proliferation in moderate degree and lead to a partial resti- 
tution of muscle tissue. This, however, is usually atypical in 
structure and of little functional importance. Losses of substances 
in muscle are largely repaired, with varying functional success, by 
connective tissue. 

Specialized gland tissue, while readily enough maintaining by 
cell proliferation its integrity under the ordinary functional wear and 
tear, is incapable as a rule, by proliferation of its specially endowed 
cells, of making good extensive losses of substance, either from 
injury or destructive pathological processes. It should not be under- 
stood by this that healing and a general restoration of the part may 
not occur after extensive injuries to such organs as the liver, kidneys, 
thyroid gland, etc. ; such a general healing may occur, but it is 
largely through growth of a new connective tissue. The specialized 
gland cells, be it in the liver, kidney, salivary, or other glands, or 
in the mucous membranes, under favorable conditions are apt to re- 
spond to an injury with destruction of tissue by proliferation, or, it 
may be, by the actual production of considerable new gland tissue. 
But the new gland tissue thus produced is usually inconsiderable in 
amount, atypical in form, and often of questionable value. The 



REGENERATION, METAPLASIA. 95 

liver and the thyroid gland seem, however, to possess in an excep- 
tional degree the power of regeneration. 

We thus see that though specialized cells in the body express, in 
the face of tissue injuries, distinct recuperative tendencies, they are 
not in general able to make good extensive losses of substance. This 
is usually done by the cells of a group of tissues more lowly in or- 
ganization, but retaining largely the proliferative power of undiffer- 
entiated protoplasm, namely, the connective tissues. 1 

The formation of leucocytes appears to occur chiefly in those masses 
of lymphoid tissue which are so widely scattered in the body in the 
lymph nodes, in the spleen, and in the bone marrow. 

Both mitotic and amitotic cell division are to be observed in the 
new formation of leucocytes, but the exact relationship between the 
new cells produced in these two ways, and their respective destinies, 
is not yet very clear (see Blood). 

Regeneration of red blood cells seems to occur in the bone marrow 
through mitotic division of nucleated forms. The latter may, under 
pathological conditions, appear in the vessels in varying numbers. 

METAPLASIA. 

The members of the connective-tissue group — fibrous tissue, mu- 
cous and fat tissue, cartilage, bone, etc. — are so closely related in 
nature and structure that not infrequently and under a variety of 
conditions one form of tissue will assume the characters of another. 
This change of one form of tissue into another is called metaplasia. 

Thus, by a gradual change in the cells and stroma of fibrous tis- 
sue this may be converted into bone, as mucous tissue may become 
fat tissue, and hyalin cartilage become fibrous. Metaplasia is a 
process involving active changes on the part of the living cells of the 
tissue, and should be clearly distinguished from certain degenera- 
tive processes, in the course of which one form of connective tissue 
may assume superficial resemblances to others of the group, as in 
calcareous and mucoid degeneration. While metaplasia is most 
common among the members of the connective-tissue group, it some- 
times occurs in other tissues. Thus, for example, under certain con- 
ditions one type of epithelium may assume the morphological charac- 
ters of another. 

1 A summary of recent studies on the regenerative capacities of the nervous 
tissues maybe found in the " Ergebnisse der allg. path. Morphologie und Physiolo- 
gic, " Abth. 2, 1895. 



DEGE1N"EKATIVE CHANGES ITS' THE TISSUES. 



Necrosis. — Necrosis is the death of a circumscribed portion of 
tissue. It may be the result of insufficient nutrition from the cut- 
ting-off of the blood supply ; or it may depend upon the action of 
destructive chemical agents, extreme degrees of temperature, certain 
materials produced by the life processes of some forms of bacteria ; 
or it may be due to mechanical injury. The appearances which dead 
tissues present under the microscope vary greatly. In some cases 
we have a simple and gradual disintegration and softening of the 
tissue, resulting in a mass of degenerated cells and cell detritus, 
with more or less fluid and various chemical substances arising 
from decomposition. The softening of the brain in embolism is an 
example of simple necrotic softening. In some cases the dead tissues 
simply gradually dry and shrivel and become hard and dark colored. 

In another class of cases the dead tissues are permeated by fluids 
which may be dark red in color from the solution of coloring matter 
from the blood, and contain bacteria which induce putrefaction with 
the production of gases and various new chemical substances. The 
tissues become swollen and granular, and disintegrate ; and finally 
the whole may form a mass of irregular granules with fat droplets, 
ty rosin, leucin, and various forms of crystals, shreds of the more 
resistant kinds of tissue, and bacteria. 

Coagulation Necrosis. — If dead areas of tissue (whether this con- 
dition be due to mechanical injury, to disturbances of nutrition, or to 
the local action of bacterial or other poisons) contain the elements 
necessary for the coagulation of their albuminous constituents, or if 
they be bathed with body fluids from adjacent parts in which the cir- 
culation is maintained, a characteristic coagulation of the necrotic 
elements is apt to occur. The composition of the cells of the tissue is 
altered, so that the cell bodies are shining and translucent, dimin- 
ished in size, sometimes altered in shape, and the nuclei of the cells 
disappear. The white infarctions of the spleen and kidneys, the 
areas of coagulation necrosis in tuberculosis, and the pseudo-mem- 
brane in croupous inflammation of the mucous membranes are the 
most common examples of this lesion. 



DEGENERATIVE CHANGES IN THE TISSUES. 97 

If, for example, in the spleen, one of the small arteries is plugged 
by an embolus, a corresponding portion of the spleen becomes anaemic 
and appears as a white, wedge-shaped mass, sharply defined from the 
surrounding splenic tissue. If such a white infarction has existed 
but a short time there is hardly any difference between the appear- 
ance of its anatomical elements and those of the surrounding spleen, 
except that they are differently affected by staining fluids. If the 
infarction is older the cells are small and shiny and their nuclei can- 
not be seen. 

In croupous inflammations of mucous membranes the epithelial 
cells become shiny, the nuclei disappear, and the shape of the cells is 
changed by the coagulation necrosis, so that a number of them 
together often look like a network of coagulated fibrin. 

Cheesy Degeneration. — As commonly used this term embraces 




Fig. 9.— An* Area of Cheesy Degeneration (Coagulation Necrosis) in Miliary Tubercle 

of Lung. 

the changes in the tissues which we have just considered under the 
more appropriate name of coagulation necrosis. But it is also applied 
to that form of degeneration in which, under a variety of conditions, 
the dead tissue elements lose their normal structural features and 
become converted into an irregularly granular albuminous and fatty 
material which sometimes tends to disintegrate and soften, sometimes 
dries and becomes dense and firm, or may become infiltrated with 
salts of calcium. Thus cheesy degeneration may, and very often 
does, occur in tissues which are in the condition of coagulation necro- 
sis; but it also occurs in tissues which are not the seat of coagulation 
necrosis, but which, for a variety of reasons and in a variety of ways, 
have lost their vitality. 

The terms coagulation necrosis and cheesy degeneration, as com- 
monly used, in part actually cover the same degenerative conditions 
in the tissues. Both are indefinite, and will no doubt remain so until 



98 DEGENERATIVE CHANGES IN THE TISSUES. 

we obtain a more precise knowledge of the lesions which they 
represent. 

Parenchymatous Degeneration (Acute Degeneration; Granular 
Degeneration; Cloudy Swelling). — In this condition the cells of tis- 
sues and organs are swollen and filled with small albuminous gran- 
ules, which may be so abundant as to entirely conceal the original 
cell structure. The granules disappear on treatment with acetic acid, 
and are insoluble in ether. This degeneration may be present in the 
parenchyma cells of any inflamed organ, but is most marked and fre- 
quent in the liver, kidney, heart muscle, and mucous membrane of 
the gastro-intestinal canal. It may occur in infectious or severe 
febrile diseases, after severe burns, and in poisoning with arsenic, 
phosphorus, or mineral acids. It is often associated with various 
phases of exudative inflammation. The cells in a condition of paren- 







Fig. 10.— Fatty Degeneration of Heart Muscle. 

chymatous degeneration may regain their normal condition, or be- 
come fatty, or disintegrate. In such organs as the liver, kidney, and 
heart the gross appearances are often very characteristic ; the tissue 
is swollen and has a less translucent and more dull and grayish look 
than under normal conditions. 

The microscopical study of this lesion is best clone in sections of the fresh tissue 
made with the freezing microtome, by the rapid formalin method, page 51, or in 
teased fresh tissue in one-half-per-cent salt solution. 

Fatty Degeneration. — This is the conversion of the protoplasm 
of cells into fat, which accumulates in the cell body. The fat is usually 
present in the cell in very small particles or droplets, but these may 
coalesce to form large drops. The protoplasm may even be almost 
entirely replaced by the fat. 

Fatty Infiltration of cells is a common occurrence under normal 
as well as pathological conditions. The fat is believed to originate 
outside of the cells and simply accumulate in them, causing a passive 
atrophy of the protoplasm. In this way fatty infiltration is believed 



DEGENERATIVE CHANGES IN THE TISSUES. 99 

to differ essentially from fatty degeneration, but in many cases a 
definite distinction between the two is impossible with our present 
knowledge of the chemistry of cell life. In general the fat droplets 
are larger in fatty infiltration than in fatty degeneration, yet to this 
there are many exceptions. Fat granules and droplets are recog- 
nized in cells by their strong refraction, by their solubility in alcohol 
and ether and their insolubility in acetic acid, and by the black 
color which they assume when the fresh tissue is treated with osmic 
acid. Not infrequently feathery clusters of delicate fat crystals 
occur within the cells. Fatty -degenerated cells may break down and 
form an oily detritus, in which, especially when much moisture is 
present, cholesterin crystals may be formed by decomposition of the 
fat. 

To the naked eye, organs in a condition of marked fatty degenera- 




Fig. 11.— Fatty Infiltration op Liver Cells. 

tion are usually larger and softer than normal, have a grayish-yellow 
color or are mottled with 3-ellowish streaks or parches, and the nor- 
mal markings of cut surfaces are more or less obscured. 

Fatty degeneration may be due to local or general disturbances 
of nutrition, from a great variety of causes — disturbances which 
either directly affect the life processes of the cells themselves, or 
which produce alterations in their nutritive supply. In addition to 
its local occurrence, as a result of local disturbances of circulation, in 
the vicinity of inflammations or in tumors, etc. , it is apt to occur in 
the liver, heart muscle, and kidney in chronic exhausting diseases 
and in conditions and diseases to which profound anaemia is incident, 
or as the result of the action of certain poisons, such as phosphorus 
and arsenic. Fatty degeneration is, as a rule, a more serious lesion 
than fatty infiltration. 

Tissues in a condition of fatty degeneration or infiltration may be teased fresh in 
salt solution ; or they may be hardened in Flenvming's osmic acid solution, see page 



100 DEGENERATIVE CHANGES IN THE TISSUES. 

54, in preparation for sectioning. Hardening in Miiller's fluid and afterward in 
alcohol gives moderately good results if the lesion be extensive. But it should be 
remembered that in tissues which have been soaked in alcohol the fat is no longer 
present, its former seat being indicated by clear spaces which are filled with the 
mounting medium. The fat crystals, however, often persist after prolonged soak- 
ing in alcohol. 

Amyloid Degeneration (Waxy or Lardaceous Degeneration). — 
This is a process by which the basement substance of various forms 
of connective tissue, and especially the walls of the blood vessels, be- 
come swollen and thickened by their conversion into a translucent, 
firm, glassy, colorless material, albuminous in character. This albu- 
minous material may be present in the tissues in such small amount 
as to be recognizable only under the microscope, or it may be so 
abundant as to give a very characteristic appearance to the tissue. 
Parts in which the lesion is marked are usually larger and contain 
less blood and feel harder than normal, and have a peculiar dull 
shining and translucent appearance which varies in character, de- 
pending upon the extent and distribution of the degenerated areas 
and upon its association with other lesions, such as fatty degenera- 
tion. It most frequently occurs in the smaller arteries and capillaries, 
whose lumen becomes encroached upon by the thickening of the 
walls which the process involves. It is usually the media and inter- 
mediary layers of the intima which are earliest and most extensively 
affected. The change also often occurs in the interstitial connective 
tissue and membranae propriae of organs and in reticular connective 
tissue. It is both asserted and denied that it may affect the paren- 
chyma cells of organs. We have not been able to find unmistakable 
evidence of its occurrence in parenchyma cells. These, however, 
frequently undergo atrophy as the result of pressure from the swol- 
len, degenerated tissue. 

It is not yet known whether amyloid degeneration is due to a 
direct transformation of the tissue, or is an infiltration of the tissue by 
some abnormal material formed elsewhere and brought to it, or is de- 
rived from the blood. 

Amyloid degeneration occurs most frequently and abundantly in 
the liver, spleen, kidneys, intestinal canal, and lymph nodes; but it 
may occur, usually in a less marked degree, in other parts of the 
body : in the larger blood vessels, in the interstitial tissue of the 
heart and mucous membranes of the air passages, and in the genera- 
tive organs. It may occur locally or appear in various parts of the 
body at once. It may exist without any known cause, but it most 
frequently occurs in connection with severe wasting diseases, par 
ticularly in those involving chronic suppuration and ulceration, espe- 
cially of the bones. It frequently occurs in tuberculosis, syphilis. 



DEGENERATIVE CHANGES IN THE TISSUES. 



101 



in the cachetic condition induced by malignant tumors, and is 
occasionally seen in severe malarial infection, dysentery, and leu- 
kaemia. 

For microscopical examination, the tissue, either fresh or after preservation, 
should be cut into thin sections, and these deeply stained with one-per-cent aqueous 
solution of methyl violet ; the sections are washed in water and mounted in glycerin. 
The differentiation between the amyloid and other parts is more distinct if, after 
staining, the specimen be dipped for an instant in HC1 and alcohol 1:100, and 
then carefully rinsed, before mounting in glycerin. The degenerated areas are thus 
stained rose-red (Fig. 12), while the normal tissue elements have a bluish-violet 
color. In some cases, for reasons which we do not know, the amyloid substance 
does not show a well-marked reaction with methyl violet. A sharp differentiation 
of the amyloid material may be obtained by picro-acid fuchsin (Van Gieson's stain) , 
page 61. Other anilin dyes also differentiate amyloid substance from normal tis- 
sues. On treating sections of amyloid tissue with solution of iodine the degenerated 




Fig. 



12.— Amyloid CWaxy) Degeneration op Capillaries op a Glomerulus in the Kidney. 
A, waxy capillaries stained with methyl violet; B, normal capillaries. 



parts acquire a mahogany color. If they are then treated with sulphuric acid the 
degenerated portions acquire a greenish or blue color ; but the latter reaction is not 
very reliable. 

Corpora Amylacea are small, spheroidal, homogeneous or lam- 
ellated bodies (Fig. 13) , which assume a bluish color on treatment with 
solution of iodine or iodine and sulphuric acid. They are frequently 
found in the acini of the prostate gland, sometimes in large numbers; 
in the ependyma of the ventricles of the brain, and in areas of 
sclerosis of the brain and cord ; also in extravasations of blood and in 
various other situations. They may occur under normal as well as 
pathological conditions, and are apparently of little importance. 
They seem to have nothing to do with amyloid degeneration, although 



102 



DEGENERATIVE CHANGES IN THE TISSUES. 



they somewhat resemble its products. Some of the tube casts of the 
kidney resemble in many respects the corpora amylacea. 

Glycogen Degeneration. — Glycogen appears under abnormal 
conditions in the body as hyalin, mostly globular masses of varying 
size. It is soluble in water, is stained brownish-red by iodine, and 
does not assume a greenish color by the further addition of sulphuric 




Fig. 13.— Corpora amylacea. 
From prostate gland. 



acid. In diabetes it may occur in large quantities in the liver cells 
and in the epithelial cells of the uriniferous tubules, especialty in 
those of Henle's loop and in leucocytes. It may be found in fresh 
pus cells, in the cells of various forms of tumors, and in leucocytes in 





Fig. 14.— Mucous Degeneration of Epithelial Cells. 
From cyst adenoma of ovary. 

the blood in leukaemia, in chronic diseases of the gastro-intestinal 
tract in children, and in various chronic diseases. 

If the tissue to be examined for glycogen be fresh the iodine should be used in 
solution in glycerin (equal parts of Lugol's solution and glycerin) , in order to avoid 
its solution. If specimens are to be hardened this should be done in absolute alcohol 
to avoid the solution of the glycogen. Sections may be stained with picro-acid 
fuchsin (Van Gieson's stain) or with a dilute solution of iodine in alcohol (tincture 
iodine 1 part, absolute alcohol 4 parts), cleared up and studied in oil of origanum. 

Mucous Degeneration may occur in cells or in intercellular sub- 
stance. When occurring in cells it consists, under pathological as 
under normal conditions, of the transformation of the protoplasm 



DEGENERATIVE CHANGES IN THE TISSUES. 103 

into a translucent, semi-fluid material, occupying more space than the 
unaltered protoplasm, and hence causing a swelling of the cells (Fig. 
14). This new-formed material contains mucin in solution, which 
is precipitated by acetic acid. It occurs under a variety of condi- 
tions, sometimes as a morbid increase of a normal function of cells, 
as in many catarrhs, sometimes as an entirely abnormal transforma- 
tion. The cells may be entirely destroyed by the accumulation of 
the mucoid material within them. s 

In certain cases, as in many tumors, in cartilage, bone, and other 
tissues, the intercellular substance undergoes conversion into mucin- 
containing material, losing almost entirety its original structure 
(Fig. 15). The cells in such cases may be affected only secondarily 
by the pressure which the new-formed material exerts upon them. 



■\-t 



f - A v ^m , ft; 









y 







Fig. 15.— Mucous Degeneration of Fibrous Tissue of Mamma. 

Tissues should be hardened in Muller's fluid or formalin, followed 
by alcohol, and sections stained with picro-acid fuchsin or with 
hasmatoxylin, which colors the mucin-containing portions. 

Colloid Degeneration is very closely allied, both in chemical and 
morphological characters, to mucous degeneration, and in many 
cases there is no definite microscopical distinction between them. 
But colloid material is firmer and more consistent than mucous, does 
not yield a precipitate on addition of acetic acid or alcohol, and its 
formation is usually confined to cells; not involving intercellular sub- 
stance, except by an atrophy which its accumulation sometimes 
induces. The cells may contain larger and smaller droplets of colloid 
material (Fig. 16), or it may nearly or entirely replace the protoplasm 
and accumulate to such an extent as to cause rupture and destruction 
of the cell. In this way, and by the atrophy of intercellular sub- 
stance which its accumulation causes, cysts may be formed contain- 



104 



DEGENERATIVE CHANGES IN THE TISSUES. 



ing colloid material and cell detritus. Colloid degeueration is of 
frequent occurrence in certain tumors and in the thyroid gland, and 
occurs occasionally in other places. 








«-' 



^%r. 




Fig. 16 — Colloid Degeneration of Epithelial Cells. 
From carcinoma of rectum. 

Hardening in formalin, Muller's fluid, or alcohol. Staining 
with picro-acid fuchsin. 

Hyalin Degeneration is the transformation of tissues into a 
transparent, glassy substance, much resembling amyloid in its mor- 




Fig. 17.— Hyalin Degeneration of Capillary Blood Vessels. 
From a sarcoma of the optic nerve. 

phological characters (Fig. 17) ; but it does not give the micro- 
chemical reactions of amyloid, and appears under different condi- 
tions. Hyalin substance is quite resistant to the action of acids and 
stains readily with acid fuchsin and eosin. It occurs especially in 



DEGENERATIVE CHANGES IN THE TISSUES. 



105 



the walls of the smaller blood vessels in various parts of the body, in 
voluntary muscle fibres, and is said to sometimes involve interstitial 
tissue. It has been described as occurring in the brain, lymph nodes 
and ovaries ; in the tubules of the kidney, in the walls of aneurisms, 
in muscle fibres, in the lesions of diphtheritis, tuberculosis, and 
syphilis, in the hyaloid membrane and vessels of the eye, and else- 
where. It is sometimes called vitreous or fibrinous, and also waxy, 
degeneration. It is believed by some observers that fibrin, blood 
plates, and leucocytes may undergo hyalin degeneration, and in the 
forms of the so-called hyalin thrombi this substance may block the 
capillaries in many infectious diseases — typhoid fever, pneumonia, 
diphtheria, pysemia, etc., and under a variety of other conditions. 
Hyalin degeneration seems to be, in some ways, allied to coagulation 



"> ::; %S^li^^*^^C : %%^''^ 



^: 



fe^Cm 1 ifei& 




Fig. 18.— Pigmentation of Connective-tissue Cells of the Lungs. 
From inhaled coal dust— anthracosis. 



necrosis, but its exact significance and relations to other forms of de- 
generation, and the conditions of its occurrence, are not yet known. 1 

Hardening in alcohol, Miiller's fluid, or formalin. Staining by 
picro-acid fuchsin, or by hematoxylin and eosin. 

In Calcareous Degeneration there is a deposition, either in cells 
or in the intercellular substance, of larger and smaller granules com- 
posed chiefly of phosphate and carbonate of calcium. These particles, 
when abundant, give hardness, brittleness, and a whitish appearance 
to the affected tissue. Under the microscope they appear dark by 
transmitted, white and glistening by reflected, light. Tissues may 
be nearly completely permeated with the salts, or the latter may be 
scattered in patches through them. Sometimes large lamellated con- 
cretions are formed in tissues, usually at the seat of some old inflam- 
matory process. Calcification usually occurs in parts of tissues which 



1 Consult "Ergebnisse der allg. 
Abth. 2, 1895. 




path. Morphologie und Physiologie, " etc., 



106 DEGENERATIVE CHANGES IN TISSUES. 

are dead or are in a condition of reduced vitality as a result of 
some antecedent morbid process, usually of an inflammatory nature. 
Among the most common and important examples of calcareous 
degenerations may be mentioned those which occur in the valves of 
the heart and walls of the blood vessels. 

The carbonate of lime deposited in the tissues is dissolved by dilute acids with 
evolution of carbonic acid gas. 

This process may be observed under the microscope by running five per cent 
hydrochloric acid under the cover glass upon unstained sections ; the gas bubbles are 
caught as they evolve beneath the cover. Those parts of tissues which are in an 
early stage of calcification, as well as those from which the lime has been removed by 
acids, are usually stained an intense blue by hematoxylin. 

Pigmentation. — The pigment which is present in the body under 
abnormal conditions may be formed in the body or may be introduced 
into it from without. It may be deposited in the cells or in the 
intercellular substance, and is sometimes visible to the naked e} T e and 
sometimes not. The pigment occurring in the body may be in the 
form of yellow, brown, black, or reddish granules or in crystalline 
form. In the majority of cases it is formed by the decomposition of 
haemoglobin from extravasated masses of red blood cells. Parts which 
have been the seat of long-continued hyperasmia may have a diffuse 
grayish appearance from the alteration of the haemoglobin in red 
blood cells which have escaped from the vessels by diapedesis. Pig- 
ment may be formed in the blood vessels in severe cases of malarial 
infection, and circulate in the blood. In another class of cases 
various forms of cells seem to be actively concerned in elaborating 
pigment; this is exemplified in the true melanotic tumors, and the 
process has its physiological prototype in the formation of pigment 
in the choroid, skin, and some connective tissues. Pigmentation of 
tissue from the bile occurs under a variety of conditions, and may be 
the result of the deposition of granules or crystals. A diffuse stain- 
ing also frequently occurs from the bile without the formation of 
solid particles. 

In many cases the mode of formation of pigment is not at all 
understood. In tissues which are normally somewhat colored the 
color may greatly deepen by a simple atrophy of the tissue without 
the new formation of pigment, as in simple atrophy of the heart 
muscle and in atrophied fat. 

As examples of pigment introduced into the body from without, 
we may mention the deposition of minute particles of silver from the 
internal use of silver nitrate; the coloring of the skin and lymph 
glands from tattooing; and especially the pigmentation of the lungs 
and bronchial glands (Fig. 18) from the inhalation of coal and other 
dust, which is universally present under the conditions which modern 
civilization imposes. 



INFLAMMATION. 



The phenomena which are embraced under the name of inflam- 
mation are : 

Degeneration and death of tissue. 

Changes in the circulation of the blood. 

Escape of the elements of the blood from the vessels. 

Formation of new cells and new tissue. 

These morbid changes either occur separately or are combined in 
various ways. 

The growth of the body of pathogenic micro-organisms and the 
formation by them of toxic substances is a frequent inciting cause of 
inflammation. 

We have therefore to consider first, separately : Degeneration and 
Necrosis; Congestion, Transudation, and Emigration; the Produc- 
tion of New Cells and Tissues ; the Presence and Action of Micro- 
organisms ; and secondly, the different combinations of the various 
phases of inflammation. 

DEGENERATION AND NECROSIS. 

Degeneration. — This change, which is limited to the parenchyma 
cells of the viscera and to the nerve and muscle fibres, is always caused 
by the presence of some toxic substance. The poison may be an 
inorganic one, such as arsenic, phosphorus, or mercury ; or it may be 
an organic one, such as is often produced in the growth of pathogenic 
micro-organisms. 

The microbic poisons of the different infectious diseases vary as to 
the parts of the body which they especially affect. In all the infec- 
tious diseases the renal epithelium is especially vulnerable and seldom 
escapes degeneration. 

The changes in the cells vary with the virulence and the quantity 
of the poison introduced into the body. A mild poisoning onry pro- 
duces an increase in the size of the cells and a change in their com- 
position, so that they are more opaque and more coarsely granular. 



108 INFLAMMATION. 

This change in the cells is not necessarily attended with any evident 
disturbance of their functions. If the poison be withdrawn, the cells 
return to their normal condition. 

A more severe poisoning not only causes the cells to become 
swollen, but they are also infiltrated with granules of albuminoid 
matter and of fat, and some of them disintegrate and break down. 

In the more intense forms of poisoning there is a rapid death of 
the cells. They either disintegrate and break down, or pass into the 
condition of coagulation necrosis. 

When the degeneration of the cells is marked and rapid there are 
often added congestion of the blood vessels, exudation of serum, and 
emigration of white blood cells. 

The severe forms of degeneration cause disturbance or abolition of 
the functions of the cells of the viscera. Degeneration of the nerve 
fibres may produce motor paralysis and pain. Degeneration of the 
voluntary muscles may be followed by their rupture. The interfer- 
ence with the functions of the viscera and the paralysis may cause 
death. If the patients recover, the degenerated cells are replaced by 
new cells of the same kind. 

Necrosis. — The ordinary causes of death of tissue are: a cutting 
off of the blood-supply, the direct action of caustic substances; 
extreme heat or cold ; severe concussions, and the poisons developed 
in the growths of pathogenic micro-organisms. 

The dead tissue is either changed into a mass of amorphous 
granules, or the cells pass into the condition of coagulation necrosis. 
The area of dead tissue may afterward shrink, be absorbed, and 
finally disappear; it may remain indefinitely in the condition of coag- 
ulation necrosis; it may soften, break down, and form a cavity; or 
it may undergo putrefaction. 

Such a necrosis of tissue may occur as an isolated process without 
changes in the surrounding tissues. Much more frequently there are 
associated with it congestion and infiltration of the surrounding 
tissues with the serum, fibrin, and pus. 

These changes around the portion of dead tissue seem to be due 
partly to the irritation caused by dead tissue, partly to the presence 
of micro-organisms. In the necrotic forms of inflammation there is 
often a mixed infection. 

CONGESTION, TRANSUDATION, AND EMIGRATION. 

Congestion. — The blood vessels, especially the capillaries and 
veins, in any part of the body may for a shorter or longer time con- 
tain an increased quantity of blood. This part of the body is then 
said to be in the state of active or chronic congestion. 



INFLAMMATION. 109 

Either active or chronic congestion interferes with the functions 
of the viscera. 

Active congestion is often followed by exudative inflammation. 

Chronic congestion is often followed by productive inflammation. 

Transudation. — During life in the human body there is a con- 
stant escape of the fluid constituents of the blood from the capillaries 
into the lymph spaces and an absorption of the fluid from the lymph 
spaces by the lymphatic vessels. If the equilibrium between transu- 
dation and absorption is disturbed the fluid accumulates in the lymph 
spaces and serous cavities. When such an accumulation of fluid 
occurs with inflammation it is called an exudate, when it occurs 
under other conditions it is called an oedema or dropsy. 

Emigration. — The escape of the white blood cells from the capil- 
laries and veins is usually associated with the transudation of blood 
serum, but may occur without it. 

One cause for emigration is the presence in the tissues near the 
blood vessels of substances produced by bacteria which are positively 
chemotactic — that is, of substances which attract white blood cells 
toward them. 

It is also found that a variety of irritating substances in the 
tissues are capable of causing an emigration of white cells. Appar- 
ently whenever the emigration of white blood cells is very large it is 
due to the presence of pathogenic bacteria, especially the streptococci 
and staphylococci and the pneumococci. 

The white blood cells which have emigrated into the tissues may 
remain for a time as pus cells and afterward degenerate and be 
absorbed. Furthermore, these cells are capable of taking into them- 
selves bacteria as well as other foreign bodies, and in this way they 
may be of use in limiting infection. 

It is also to be noticed that when an extensive local emigration 
of white blood cells is caused by bacteria there may be at the same 
time an increase in the number of white cells in the blood throughout 
the bodj- — leucocytosis. 

PRODUCTION OF NEW CELLS AND TISSUES. 

With or without other inflammatory changes, there may be a 
production of new cells and a growth of new tissue. When new 
tissue is formed it usually follows the type of connective tissue, 
consisting of cells of various forms and sizes and of a more or less 
fibrillar basement substance. 

This new tissue may be called granulation tissue, round-celled 
tissue, indifferent tissue, connective tissue, fibrous tissue, tubercle 
tissue, etc. 



110 INFLAMMATION. 

As a rule the more acute the process the greater the number of 
cells ; the more chronic the process the greater the quantity of base- 
ment substance. 

In an acute inflammation the production of new tissue may occur 
by itself, but is more frequently associated with exudation. In 
chronic inflammation the growth of new tissue is often not attended 
with congestion or exudation. 

Whenever in any inflammation there is at the first a production 
of new tissue, that inflammation regularly goes on to assume the sub- 
acute or chronic form. 

The Relation of Micro-organisms to Inflammation is con- 
sidered in the section devoted to the Infectious Diseases. 

FORMS OR PHASES OF INFLAMMATION. 

In classifying and naming the different forms of inflammation 
it is convenient to name them according to the most prominent of 
the different changes which go to make up the whole process. We 
distinguish : 

1. Exudative Inflammation. 

2. Productive Inflammation. 

(a) Simple Acute Productive Inflammation. 

(b) Productive Inflammation with Exudation. 

(c) Chronic Productive Inflammation. 

3. Necrotic Inflammation. 

1. Exudative Inflammation. — An exudative inflammation is 
one characterized by the presence of an exudate — serum, fibrin, and 
pus. The production of such an exudation may or may not be 
attended with marked changes in the inflamed tissues. The process 
may run an acute, a subacute, or a chronic course. The structure 
of the inflamed tissue, whether connective tissue, a mucous mem- 
brane, or a viscus, modifies the character of the inflammation. 

The most characteristic and common of the exudations are 
serum, fibrin, and pus. In order to understand the way in 
which these are produced and the varied post-mortem appearances to 
which their presence gives rise, it is well at the outset to study some 
variety of exudative inflammation in actual occurrence in a living 
animal. The frog is the most convenient animal for this purpose. * 

If we expose the mesentery or bladder of the frog so that we can 
study it under the microscope, marked inflammatory changes soon 
occur without other inciting agency than is furnished by the changed 
position and exposure to the air. At first the arteries, veins, and 

ir That essentially the same phenomena occur in the warm-blooded animals as in 
the frog has been shown by the studies of Tlioma and others. 



INFLAMMATION. 



Ill 



capillaries dilate, and the blood, encountering less resistance from 
the walls, flows more rapidly through them. This increased rapidity 
of the blood current does not, however, last long, although the ves- 
sels still remain dilated. After a variable period, owing, it is be- 
lieved, to changes of the inner surface of the vessels, the blood meets 
with so much resistance that it now flows more slowly than under 
normal conditions. Temporary or even permanent stasis may occur 
in some of the vessels, but this is not a constant nor characteristic 
occurrence. White blood cells — leucocytes — now begin to accumu- 
late along the inner walls of the veins and to become fixed there, so 
that after a time the whole inner surface of the veins may be more 




Fig. 19 —Emigration op White Blood Cells in Inflamed Bladder of Frog. 



or less thickly sprinkled, and even closely crowded, with adherent 
leucocytes. These may either lie firmly against the endothelium or 
be dragged slowly along by the current of blood sweeping past them. 
Some are dragged by the blood current into pyrif orm shapes, show- 
ing that they are adherent only at a small point, and thus they may 
be detached from the wall and rejoin the circulating blood. In the 
capillaries, also, leucocytes may be seen clinging firmly to the wall. 
After a time, which varies considerably — in the bladder some- 
times within an hour after its exposure ; in the mesentery usually 
much later — some of the leucocytes commence to make their way 
slowly through the walls of the veins and capillaries. At first a little 



112 INFLAMMATION. 

shining knob appears on the outside of the wall opposite to the cell 
which is sticking within, and this outer portion grows larger and 
larger as the part still within grows smaller, until at length the en- 
tire cell is outside of the vessel. The cell now may immediately de- 
tach itself and wander off in the lymph spaces, or it may remain for 
some time attached to the outside of the wall. This passage of the 
leucocytes through the walls of the capillaries and veins — it does not 
occur in the arteries — is called emigration. The emigrating cells 
are, largely at least, the polynuclear leucocytes (see page 82). 

The cells pass between the endothelium through the cement sub- 
stance, which becomes in some way changed in the inflammatory 
process. They may pass through very rapidly, but usually their 
progress is slow and often interrupted, so that cells may be seen 
motionless for a long time in various stages of progress through the 
walls. A half -minute, or even less, may suffice for their passage, 
or they may be hours about it. Thus, after a variable time, if the 
conditions have been favorable, the tissues immediately around the 
capillaries and veins, and even those somewhat remote from them, 
may be more or less densely crowded with leucocytes, some motion- 
less and in the spheroidal form, others moving about through the 
lymph spaces. Leucocytes may pass out of the tissues on to free 
surfaces of the inflamed part. 

It is probable that the emigration of the leucocytes is due in part 
to a sort of filtration process with which the pressure of the blood 
within the vessels is concerned. But the inherent contractility of 
the cells themselves forms, doubtless, a very important factor. 

While this is going on the red blood cells, although for the most 
part carried in the usual way along in the axial current of the veins 
and through the capillaries, still usually find their way, in small, but 
sometimes in very large numbers, through the walls of the veins and 
capillaries into the surrounding tissues. They are, it is believed, 
carried passively through the cement substance between the endo- 
thelium by currents of fluid which under these conditions are flow- 
ing in abnormal quantities through the walls. This extravasation 
of the red blood cells is called diapedesis. 

By this time it will usually be found that the tissue around the 
vessels is somewhat swollen and more succulent than normal, and 
fluid may be poured out on the free surface. 

The fluid which is thus formed is called serum, and it is some- 
what similar to simple non-inflammatory transudation, except that it 
contains more albumin and is mixed with cells. This serum has evi- 
dently passed out of the blood vessels along with the blood cells, and, 
as its composition differs somewhat from that of blood plasma, it is 
evident that it has undergone some sort of change as it passed 



INFLAMMATION. 



113 



through the cement substance of the endothelium. The way in 
which this alteration in the composition of the blood plasma occurs 




Fig. 20. — Exudative Inflammation— Exudate in Air "Vesicle of the Lung in Lobar Pneumonia 
Showing fibrin, pus ceils, red blood cells, and epithelium. 



'.MMsSMrAMxf 




Fig. 21.— Exudative Inflammation in the Wall of the Appendix Vermiformis. 
Showing extravasated leucocytes in the vicinity of the blood vessels with oedema of the sur- 
rounding connective tissue. (Specimen loaned by Dr. Ely). 

as it passes through the walls of the vessels and becomes the serum 
of exudation, we do not understand. 

10 



114 INFLAMMATION. 

The fluid exudate contains fibrinogenous substance, and from 
this, when the conditions are favorable, fibrin may be formed by a 
change similar to that which occurs in the coagulation of the blood. 

Thus in the living animal we can learn by direct observation 
the way in which serum, fibrin, and cells get into the tissues and 
upon free surfaces in inflammation. The fate of these exudations 
will be considered further on. 

Under certain conditions diapedesis occurs so extensively that the 
extravasated red blood cells form a very important part of the exu- 
dation, and when this occurs it constitutes the hcemor?'hagic variety 
of exudative inflammation. 

Under varying conditions, furthermore, which depend partly upon 
the seat of inflammation, partly upon its intensity, but oftener 
upon conditions which we do not understand, sometimes one, some- 
times another of the exuded materials preponderate, and we may 
thus have varieties of exudative inflammation which we call serous, 
purulent, or fibrinous; or we may have various combinations of 
these. 

It is in connective tissue that a simple exudative inflammation 
is seen in its most typical form. The structure of connective tissue 
is simple — a basement substance, cells, blood vessels, lymphatics, and 
nerves. The inflammation is attended with an increased quantity of 
blood in the vessels, more or less swelling of the basement substance 
and cells, and exudation in the natural cavities of the tissue. 

The structure of the mucous membranes is more complex. They 
are all composed of a layer of epithelium, of a connective-tissue 
stroma containing the blood vessels, nerves, and lymphatics, and of 
glands which produce mucus. The inflammation not only causes 
congestion and exudation into the stroma, but there are also changes 
in the epithelium and in the glands. In the epithelium there is a 
more active desquamation of old cells and growth of new cells ; mu- 
cus may be formed within the epithelial cells, sometimes superficial 
ulcers are formed. The function of the mucous glands is interfered 
with. At first the production of mucus is stopped, later it is in- 
creased and altered. The increased production of mucus is regu- 
larly attended with a diminution of the congestion and swelling of 
the mucous membrane. Such an inflammation in a mucous mem- 
brane is often called "acute catarrhal inflammation." ' 



1 The term catarrhal inflammation is, however, often used differently. Thus 
Ziegler says that escape of fluid on the surface of a mucous or serous membrane 
gives the picture of a serous catarrh ; if the fluid exuded on the surface of a mucous 
membrane is associated with marked mucoid change of the superficial epithelium 
and of the mucous glands it is a mucous catarrh ; if the secretion is mixed with 
much epithelium, it is a desquamative catarrh. 



INFLAMMATION. 115 

The viscera are composed of a connective-tissue stroma containing 
the blood vessels, lymphatics, and nerves, and of cells. The cells are 
peculiar to each viscus, and are concerned in performing the func- 
tions of the viscus. 

The principal changes effected by the inflammation are the con- 
gestion and consequent swelling and the inability of the visceral cells 
to perform their proper functions. The quantity of exudation may 
be small or large. 

The changes in the blood vessels and tissues which belong to exu- 
dative inflammation are produced by a variety of causes, and these 
causes seem to act primarily either on the tissues or on the blood 
vessels. 

Heat and cold seem to act directly on the blood vessels, producing 
first congestion and then exudation. Chemical irritants act first on 
the tissues and through these on the vessels. 

The different inorganic poisons and the toxins of bacteria may 
circulate in the blood and irritate the vessels from the inside, or they 
may be situated in the tissues and irritate the vessels from the out- 
side. 

The character of the exudation, whether serum, fibrin, or pus, cor- 
responds to the character of the irritant which causes the inflamma- 
tion. Thus we find that the toxin of cholera causes large exudations 
of serum, that of pneumonia a large production of fibrin, that of 
cerebro-spinal meningitis a considerable emigration of white blood 
cells. 

We have now to consider what becomes of these exudations and 
,of the degenerated and proliferated cells. Mucus usually passes 
•off on the surface with other exuded materials, but may collect in 
•considerable quantities in the cells in which it is formed or in the 
acini and ducts of the mucous glands. The extravasated red blood 
cells lose their haemoglobin, which decomposes and may be absorbed 
or deposited as granules or crystals in the tissues, while the cells 
themselves disintegrate and are absorbed. The serum may pass 
off on free exposed surfaces, or in a short time be taken again 
into the circulation by means of the lymph channels; or it may accu- 
mulate in serous cavities, where it may remain for a long time, 
mingled with other exudations. The fibrin may form in such dense 
masses in the interstices of the tissues as to interfere with their nutri- 
tion, and thus circumscribed portions of tissue may die and be ab- 
sorbed or thrown off as sloughs with their contained fibrin. Fibrin 
may disintegrate and be finally entirely absorbed, it may be thrown 
off on exposed surfaces, or it may be gradually replaced by a new- 
formed vascular organized membrane or mass of tissue, the ab- 
sorption of the fibrin going on hand-in-hand with the formation of 
the new tissue. 



116 



INFLAMMATION. 



The fate of the leucocytes varies greatly and is in many respects 
still obscure. A certain number of them, after leaving the blood 
vessels, wander through the tissues, and, entering the larger lymph 
vessels, again join the circulating blood. Others, there is reason to 
believe, undergo proliferation and thus add to the number of the 




Fig. 22 — Pus Cells from Catarrhal Inflammation of Bronchial Mucous Membrane. 

infiltrating cells. Still other leucocytes die, either in the interstices 
of the tissues or after passing on on free surfaces ; they may then 
disintegrate and be absorbed, or they may collect in masses with 




Fig. 23.— Omentum of Dog, showing Peritonitis on Fourth Day, X 500 and reduced. 

other exudations in internal cavities, or they may collect in circum- 
scribed masses in the interstices of the tissues, and, in connectior 
with other cells and more or less fluid and broken-down tissue, form 
abscesses. 

The term pus is rather loosely and indiscriminately applied to the 



INFLAMMATION. 117 

new cells which we find in the tissues in exudative inflammation, 
when these are not actually concerned in the formation of new tis- 
sue. It would be better to speak of these new cells, whose morpho- 
logical characters give us no clue to their destinies, as indifferent 
cells, and limit the term pus cells to those cells, mostly polynuclear 
leucocytes, which, produced in inflammation, have evidently died in 
or about the tissue, and which we call, in the surgical sense, pus. 

Since the great majority of new cells seen in acute exudative 
inflammation are in fact extravasated leucocytes or their progeny, 
the appearances of the ordinary pus cells are essentially the same as 
those of the leucocytes, except that they may exhibit degenerative 
changes. Thus they may present various degrees of fatty degenera- 
tion and disintegration, and the nucleus is frequently broken into 
fragments, thus simulating the commencement of proliferative 
changes. 

In exudative inflammation of the serous and mucous membranes 
we often find, in addition to the ordinary pus cells, larger and vari- 
ously shaped cells, which are detached epithelial or endothelial cells 
(Figs. 22 and 23) or the result of their proliferation. These, although 
usually present in relatively small numbers, must still be considered 
pus cells in accordance with the views above laid down. Moreover, 
we must remember that the fixed connective-tissue cells, as well as 
endothelium and epithelium, may give rise by proliferation to cells 
which resemble mononuclear leucocytes. 

2. Productive Inflammation. — (a) Simple acute productive in- 
flammation. In this form there is no exudation, no serum, fibrin, 
or pus. Congestion is sometimes, but by no means always, visible 
after death. The inflammatory product consists of new cells formed 
from the old connective-tissue cells. The pia matter and the perito- 
neum offer the best examples of this form of inflammation. 

(b) Productive inflammation with exudation. In this form of 
inflammation the changes in the blood vessels, the exudation and emi- 
gration, the formation of serum, fibrin, and pus are well marked, but 
in addition there is from the first a growth of new tissue. This new 
tissue at first consists principally of cells, later a basement substance 
and blood vessels are added. This form of inflammation has a marked 
disposition to continue for a long time in a subacute or chronic form. 

In connective tissue the serum, fibrin, and pus are found in vary- 
ing quantities. The new tissue forms thickenings and adhesions. 

In the mucous membranes the inflammation involves the stroma, 
and it is in the stroma that the exudation is infiltrated and the new 
tissue formed. The glandular coat may remain unchanged, or be 
the seat of catarrhal inflammation. 

In the viscera the quantit}' of the inflammatory product varies. 



118 INFLAMMATION. 

The new tissue is formed in the stroma. The visceral cells undergo* 
more or less atrophy or degeneration. 

The recognition of this form of inflammation with its combina- 
tion of exudation from the vessels and growth of new tissue is a 
matter of great clinical importance. It is a matter of ordinary ob- 
servation that while some inflammations of the lungs, of the kidneys, 
and of the colon run an acute course and terminate in recovery or 
death at the end of a few days, on the other hand, apparently 
similar inflammation of these organs may be protracted for weeks or 
months. A study of these inflammations in all their different stages 
shows that the key to the problem is the presence or absence of the 
growth of new tissue. The simple exudative inflammations are 
transitory in their character, and after they have subsided — if loss of 
substance have not occurred — the tissues may go back to their nor- 
mal condition. But in a productive inflammation with both exuda- 
tion and a new growth of tissue, while the exudation may stop 
and the exudate be absorbed, the new tissue is permanent and by its 
presence keeps up the disposition to long-continued inflammatory 
changes. 

(c) In chronic productive inflammation the inflammatory product 
is round-celled tissue, granulation tissue, or connective tissue. In 
some cases this is the only change ; in others there is added an exuda- 
tion from the blood vessels, or degeneration of cells. The new tissue 
that is formed may degenerate or become calcified. 

In connective tissue this form of inflammation produces thicken- 
ings and adhesions, and serum in the serous cavities. 

In mucous membranes the growth of new tissue is in the stroma. 
This is thickened, either diffusely or in the form of polypoid growths. 
The layer of epithelium may be thickened or thinned. The mucous 
glands are atrophied or hypertrophied, or become cystic. The pro- 
duction of mucus is diminished, or increased, or altered. This con- 
dition in the mucous membranes is commonly called a " chronic 
catarrhal" inflammation. 

In the viscera there is a growth of indifferent tissue, or of con- 
nective tissue, in the stroma. The visceral cells are compressed, or 
degenerated, or fatty, or disappear. The functions of the viscus are 
seriously interfered with. In the viscera this is often called an 
"interstitial" inflammation. 

The most marked features of this form of inflammation are its 
slow course and its tendency to continue. The lesions of chronic pro- 
ductive inflammation, especially in old persons, are by some believed 
to be due to chronic degeneration. 

These chronic productive inflammations constitute a large pro- 
portion of the diseases which the physician is called upon to treat* 



INFLAMMATION. 119 

Some of them follow an acute or subacute productive inflammation, 
many are chronic from the outset. 

Such inflammations may be caused by repeated irritations, such as 
we see in the lungs from the inhalations of coal and dust. They may 
be caused by the presence and growth of bacteria, as in some forms 
of tubercular inflammations. They may follow T the long- continued 
action of the poisons of syphilis, gout, rheumatism, and alcohol. 
They are often influenced by the mode of life and environment. 

3. Necrotic Inflammation. — In this form of inflammation, in 
addition to the congestion, exudation, and growth of new tissue there 
is added death of parts of the tissues in which the inflammation 
exists. This character of the inflammation is given to it by the 
presence and growth of pathogenic bacteria. Among the bacteria 
frequently present may be mentioned the Staphylococcus pyogenes 
aureus and albus, the Streptococcus pyogenes, the bacilli of diph- 
theria, of typhoid fever, and of tuberculosis. The amoeba coli is 
also a cause of necrosis. 

There is a good deal of variety as to the way in which the necro- 
sis and the other phenomena of inflammation are associated. There 
may be necrosis and very little else, as in gangrene of the lung and in 
some of the abscesses of the liver. There may be necrosis with a 
large production of pus, as in ordinary abscesses. There may be 
necrosis with a large production of fibrin, as in the croupous inflam- 
mations of the mucous membranes. There may be necrosis with a 
growth of new tissue, as in tuberculous inflammation of the lungs 
and in some of the forms of colitis. There seems in many of these 
cases to be a double infection : one form of micro-organisms producing 
the necrosis, and another the exudation, or growth of new tissue. 

When necrotic inflammation occurs in connective tissue, it is apt 
to produce abscesses. A circumscribed portion of tissue is congested, 
infiltrated with serum, fibrin, and pus, and parts of the tissue die. 
The dead tissue softens, breaks down, and cavities are formed which 
contain serum, pus-cells, and portions of dead tissue. 

In mucous membranes there are congestion, exudation of serum 
rich in fibrino-plastic substances, emigration of white blood cells, 
and necrosis of tissue. 

The fibrin infiltrates the stroma, and coagulates on the surfaces 
of the mucous membranes so as to form false membranes. The pus 
cells are entangled in the fibrin. The necrosis involves only the epi- 
thelium, which passes into the condition of coagulation necrosis, and 
forms part of the false membranes; or it involves also the stroma. 
The death of the epithelium forms superficial erosions, that of the 
stroma ulcers of varying size and depth. 

Such an inflammation of the mucous membranes is called " croup- 



120 INFLAMMATION. 

ous" or "diphtheritic." We also find with catarrhal and productive 
inflammations circumscribed necrosis of the epithelium. 

In the viscera we find congestion, exudation of albuminous 
serum, and emigration of white blood cells. In addition there may 
be degeneration or death of the visceral cells ; or death of portions of 
the stroma with groups of cells, and the formation of abscesses. 

The micro-organisms which produce necrosis also form poisons 
which permeate the entire body. So we find that persons suffering 
from this form of inflammation have a rise of temperature and other 
evidences of general poisoning. 

REPARATIVE PRODUCTION OF NEW TISSUE. 

In many cases of exudative inflammation, after the subsidence of 
the active changes in the blood vessels, the exudations are entirely 
absorbed and the tissue returns to its normal condition ; this we call 
resolution. Under certain conditions, on the other hand — for ex- 
ample, in the case of a wound with loss of substance, or in an acute 
exudative inflammation of a serous membrane where the surface is 
deprived of its normal endothelial covering, or in the healing of an 
abscess — new tissues may be formed through the agency of the new 
cells produced in the inflammatory process. 

Such inflammation with the formation of new tissue is sometimes 
called reparative inflammation, and the new tissue may be conser- 
vative and of value to the organism, as when it fills up a wound ; or 
it may be very detrimental when tissues are formed where they do 
not belong. 

Healing of Wounds. — The way in which new inflammatory tis- 
sues are formed may be best understood by following the process of 
healing in a wound with loss of substance — say, for example, a 
wound through the skin into the tissues beneath. At first there 
may be haemorrhage. After this has ceased, the injury to the tissue, 
the unusual exposure of deep-seated parts, the presence of foreign 
substances, etc., may induce the same series of events which we 
have seen occurring in exudative inflammation with production of 
serum, fibrin, and pus. The blood vessels dilate, the circulation 
becomes slower, serum transudes, and emigration sets in. Certain 
of the cells and fragments of intercellular substance near the seat 
of injury may die and in time are cast off or absorbed, the tissue 
becomes soaked and swollen by the transuded serum, and the con- 
nective-tissue cells in the vicinity may undergo proliferative or de- 
generative changes. 

After a variable time, usually on the second or third day if all 
goes well, the surfaces of the wound may be more or less covered 
with tiny red nodules called granulations. These granulations con- 



INFLAMMATION. 



121 



tain numerous thin-walled blood vessels which have sprouted out 
from the old vessels near the seat of injury, and around these a new 
loose, succulent tissue is formed, largely, if not wholly, it is believed, 
from proliferation of connective-tissue cells. On the surfaces of the 
granulations are usually a greater or less number of pus cells. 

In the formation of new blood vessels in granulation tissue there 
are at first delicate sprouts of solid protoplasm, from the cells of the 
wall of the original vessels of the part or from those which have been 
newly formed, reaching out among the exudation cells. These 
sprouts may extend for long distances and may form anastomoses 
with similar sprouts from the same or other vessels (Fig. 24). They 
consist at first of solid protoplasm, and become gradually channelled 
out by the pressure of the blood in the vessels from which they 
spring ; the blood finally entering them and forcing its way along 




Fig. 24. —Developing Blood Vessels in New-fokmed Tissue. 



them, producing a lumen as it goes. Before this channelling of the 
lumen, and hand-in-hand with its progress, new nuclei are formed in 
the protoplasm and the new-formed walls gradually assume a distinct- 
ly cellular character. At length they have well-defined endothelial 
walls, cells from without range themselves along outside of them, 
and they take their place in the vascular system of the new tissue. 
Thus, in a very short time, multitudes of new blood vessels may 
form, furnishing nutritive centres around which the organization 
of tissue proceeds. 

The cells of the granulation tissue are at first mostly small and 
spheroidal, and are usually packed pretty closely together with only a 
small amount of fluid intercellular substance. Presently some of 
the cells become larger, elongated, fusiform, or branched, and after 
a while a delicate, fibrillar intercellular substance makes its appear- 
ance about them and grows more and more abundant (Fig. 25). 



122 



INFLAMMATION. 



These larger, variously shaped cells, which appear to be formed out 
of the small spheroidal or indifferent cells of the granulation tissue, 
are usually granular, and the nucleus is usually large and distinct, 
frequently exhibiting a well-marked intranuclear network. Since, in 




Fig. 25— Granulation Tissue from Wound of Skin. 

some respects, these cells when first formed resemble some kinds of 
epithelial cells, they are often called the epithelioid cells of granula- 
tion tissue. Some of these larger cells seem to be more or less direct- 



(jb- 



■£■» v^; 




M 




&■-■ 










■ y -f'^y''' 


Wd 




/ri'~ 









y- 



,,::-?■>■ 






Fig. 26.— Fibroblasts fkom Granulation Tissue. 



ly concerned in the formation of intercellular fibres. These appear 
to develop either as filamentous branches of the cells or to be formed 
along their sides. Such fibre-forming cells are called fibroblasts 



(Fig. 26). 



INFLAMMATION. 



123 



All this time new small spheroidal indifferent cells are gathering, 
by proliferation or by continued emigration. Some of these seem to 
participate in the formation of the granulation tissue, while others, 
not finding conditions suitable for their further development, or even 
for their continued existence, die and pass off on the surface, together 
with some transuded fluid, as pus. The new tissue gradually be- 
comes more and more dense, the intercellular substance more abun- 
dant, while the cells decrease in number and become flatter and less 
conspicuous. The epithelium may now grow over from the sides and 
cover the new tissue. The new tissue, having at last undergone 
more or less shrinkage, consists of a dense, firm mass composed 
largely of fibrillar basement substance with a few flattened cells 
(Fig. 27); and with this, which is the cicatrix, the healing is com- 
plete. 

Although in the production of new tissue in connection with or 
following exudative inflammation essentially the same processes are 
involved in all cases, there are yet very marked differences in the 




Fig. 27.— Cicatricial Tissue. 



degree in which the different factors share. Thus the vascular and 
exudative phenomena may predominate and very large quantities of 
serum, fibrin, or pus be formed, while the amount of new-formed tis- 
sue may be very insignificant. In other cases the formation of new 
tissue is the dominant feature in the process, and the production of 
exudations seems to be almost entirely subordinated to this end. 

The distinction between healing by the first and second intention, 
which is of practical importance in surgery, is, from the pathologi- 
cal standpoint, only a quantitati\ r e one. For the restitution of the 
parts to the healthy condition is in both cases brought about by exu- 
dation, and proliferation of cells under the influence of vascular 
changes ; but in one case the latter changes are very slight, in the 
other more or less extensive. 

A good deal of variation is frequently seen in the formation of 
granulation tissue in the healing of wounds, as well as under other 
conditions. Thus sometimes the body cells respond but imperfectly 



124 INFLAMMATION. 

to the inflammatory stimuli, and neither cell proliferation nor blood- 
vessel growth is active. On the other hand, the development of 
blood vessels may be excessive, other tissue formation lagging behind. 
Under these conditions loops and tangles of thin- walled, contorted 
new vessels may project from the granulating surface, while useful 
tissue formation remains in abeyance (Fig. 28). The result of this 
disproportionate growth of ill-formed blood vessels is the exuberant 
granulations which the surgeon frequently removes from unhealthy 
healing surfaces. 

Cavities formed by abscesses or by necrosis in any part of the 
body maj T be filled up and their sides drawn together in a cicatrix by 
the formation of a provisional mass of granulation tissue similar in 
character to that which grows in external wounds. So, similarly, 
cysts may be obliterated and ulcers partially filled and drawn into 




Fig. 28.— Exuberant Granulations. 
From the inner surface of a granulating ovarian cyst containing pus. 

cicatricial healing. Large free surfaces, like the pleura and the peri- 
toneum, may, through the intervention of granulation tissue, pass 
from the denuded condition of an active exudative inflammation, either 
with or without, adhesions, into a condition w T hich, though by no 
means a return to the normal, we yet designate as cure. 

The so-called organization of a thrombus in a blood vessel is 
brought about by processes practically identical with those which 
have just been described in the formation of new tissue in reparative 
inflammation. The endothelial cells of the vessels and the connective- 
tissue cells in their walls proliferate, new blood vessels develop by 
sprouts from the already existing smaller vessels in their walls or 
close about them. The new cells and new blood vessels thus derived 
gradually penetrate the clot (see Fig. 73), forming new connective 
tissue, which replaces step by step the fibrin and blood which are 
gradually absorbed or removed by phagocytes. 



INFLAMMATION. 



125 



The part which the thrombus plays in its so-called organization is 
thus a wholly passive one. It acts only as a temporary supporting 
texture for the development of the new tissue derived from other 
sources which step by step replaces it. 

Some phases of the formation of fibrous tissue — such for example 
as are seen in the spinal cord after secondary degenerations in nerve 
tracts, and such as are presented by interstitial connective-tissue 
growth with atrophy of the parenchyma, in the kidney, liver, heart 
muscle, etc. — are commonly believed to be of inflammatory origin; 
but they are, on the other hand, regarded by many as fibrous hyper- 











i8fillSaKSW»s 







:';£?> 



& 







Fig. 29.— New-formed Cartilage and Osteoid Tissue from Callus after Fracture of 

the Femur. 



plasise secondary to parenchymatous atrophy and from this point of 
view may be called replacement fibrous hyperplasice. The rela- 
tionship between a chronic productive inflammation and simple 
fibrous hyperplasia, or as it is often called simple fibrosis, is still ob- 
scure, and while the result — a formation of new connective tissue 
associated with atrophy of the parenchyma in important viscera — 
is of great frequency and serious import, the determining factors in 
the change are not evident. 

Healing of Bone Fractures. — The process of healing in bone 
after fracture- is, when uncomplicated, at first similar to that in 
ordinary healing by second intention in fibrous tissue. The blood 



126 INFLAMMATION. 

and other exudates and the tissue detritus are gradually absorbed or 
disposed of by phagocytes. 1 By a proliferation of connective-tissue 
cells of the region a larger or smaller mass of granulation tissue is 
formed. This granulation tissue does not at first differ in appearance 
from similar tissue formed elsewhere in the body in the reparative 
phase of exudative inflammation. 

But soon, under the influence of the specially endowed cells of 
cartilage or bone or periosteum, but especially of the latter, the gran- 
ulation tissue becomes partially replaced either by cartilage, or by a 
substance resembling bone in general appearance, but containing no 
lime salts. This is called osteoid tissue. These new cartilaginous 
and osteoid tissues, which are apt to occur together, form irregular 
masses or interlacing trabecule in the stroma of granulation tissue. 
This constitutes the so-called callus of a uniting fracture (Fig. 29). 

Gradually, however, the osteoid tissue becomes osseous, and the 
masses of cartilage and bands of periosteal and other fibrous tissue, 
under transformations practically identical with those seen in normal 
development, are converted into bone. Thus by gradual absorption 
and reformation of bone in the usually redundant provisional bony 
mass, and by the read justment of its vascular channels, the healing, 
with more or less permanent deformity, is accomplished. 2 

1 The disposal of small foreign particles which in one way or another get into the 
body, and the removal of dead and useless fragments of tissue which may be present 
as the result of injury or disease, are cared for by larger and smaller cells, called 
'phagocytes. The cells having this matter in charge are largely leucocytes, and ail 
are apparently mesodermal lowly organized cells. Some of them are large cells and 
may be multinuclear. The disposal of dead or foreign material is accomplished 
primarily by being taken into the bodies of the phagocytes. These may either 
retain it more or less permanently, or may absorb it in virtue of their metabolic 
powers, or may carry it off to some region of deposit by the exercise of their amoe- 
boid capacities. This phagocytic action of mesodermal cells is believed to have an 
important bearing upon immunity from, and cure of, bacterial disease (see page 178) . 

2 For a more detailed consideration of the themes treated in this and the three 
preceding chapters, comprising an important section in general pathology, the 
reader may consult TJwma's "Text-book of General Pathology, " English translation 
by Bruce. 



PARASITES. 



The scope of this work permits us to do little more than enumerate 
and give a very brief description of some of the more important 
forms of animal parasites found in man. Among the vegetable para- 
sites, however, the bacteria have assumed such an important place 
in our knowledge of the etiology of certain diseases that they justly 
claim a somewhat extended consideration. 




- :■:-■■• 1/ ■■,.,.-■-" ■•-•■■'•'■■■■■■- V^£^ 

Fig. 30.— Amceba Coli. 

From the intestinal wall near an ulcer. Drawn from a specimen prepared by Prof. W. T. 

Councilman. :' ,| 



ANIMAL PARASITES. 

PROTOZOA, i 

Rhizopoda. — In this group the Amoeba coli (Amoeba dysenterica,' 
Councilman and Lafleur) is, so far as our knowledge goes, of the 
greatest pathological significance. 

It has been repeatedly found in acute and chronic dysentery, in 
the intestinal contents, at the bottom of the intestinal ulcers, and in 

1 For a resume of our present knowledge of the parasitic protozoa consult Manne- 
berg, "Ergebnisse der allg. iEtiologie der Menschlichen und Thierkrankheiten, " 
1896, p. 916. 



128 PARASITES. 

the secondary abscesses, especially of liver, which may accompany 
ulcerative colitis. The amoeba is believed to be the cause of both the 
primary ulcerative colitis and its complicating abscesses (see page 
569). 

The Amoeba coli (Fig. 30) is a single spheroidal cell, from five 
to eight times the diameter of a red blood cell, with granular proto- 
plasm and a vesicular nucleus. It often contains larger and smaller 
vacuoles. Frequently, especially when the amoeba is active, a por- 
tion of the protoplasm appears almost homogeneous — ectosarc — while 
the rest — eudosarc — is granular. When in action, in virtue of the 
amoeboid movement, it may assume various forms, thrusting out 
and withdrawing nearly homogeneous pseudopodia. It may also 
change its shape without progressive movement. It occurs in con- 
nection with acute and chronic dysentery, frequently in Egypt, 
occasionally in Russia, and is often seen in the United States. 1 




Fig. 31.— Coccidium Oviforme. 

From liver of rabbit. Showing phases in the development of the psorospermiae, which are seen 
r-, )i.raie within the capsule in C. After Braun. 

Other species of amoeba have been found parasitic in the human 
intestines. 

Sporozoa, or Gregarince. — In this group of the Protozoa some 
forms of coccidia possess well-defined pathogenic powers. The so- 
called psorospermice — minute oval structures about 0.035 mm. long, 
with a thick capsule and coarsely granular contents — which are of 
very frequent occurrence in the liver of the rabbit, forming a part of 
the contents of yellowish, irregular-shaped cysts, have been found in 
the liver, in a pleuritic exudate, and in the kidney, ureter, and heart 
muscle in man. The organism is more properly called Coccidium 
oviforme (Fig. 31), while the spores which it forms are termed 
psorospermise. 

Another, smaller form, occurring in the intestinal epithelium of 
dogs, cats, and rabbits, has been found in two cases in a similar situa- 
tion in man. 

Organisms apparently belonging in the group of Sporozoa have 

1 We refer for further details concerning the Amoeba coli to the work of Council- 
man and Lafleur on " Amoebic Dysentery, " Johns Hopkins Hospital Reports, vol. 
h\, Nos. 7, 8, 9, 1891. 



PARASITES. 



129 



been found in certain contagious epithelial growths — Molluscum con- 
tagiosnm. 

It is believed by many that Paget's disease and other somewhat 
similar skin affections are due to the presence of coccidia. 1 The 




claim that some of the carcinomata may be caused by Sporozoa has 
not as yet been sustained (see page 292). 

The Plasmodium malarial, which is believed to be the primary 
etiological factor in intermiUer ': fever, is described elsewhere. 



-^ 




Fig. 33.— Cercomonas Intestinalis. After Braun. 

The Infusoria are represented in man by several genera. 

Balantidium coli is an ovoidal organism, from 0.06 to 0.1 mm. 
long, with cilia along the sides, which occurs occasionally in diar- 
rhceal discharges in northern Europe (Fig. 32). 

Cercomonas intestinalis is a pear-shaped, flagellate structure 




Fig. 34.— Trichomonas Vaginalis. After Dock. 

(Fig. 33), about 0.012 mm. long, making, when alive, rapid move- 
ments. It has been found in the evacuations of persons suffering 
from cholera, typhoid fever, and diarrhoea. 

Trichomonas vaginalis has a oval or pear-shaped body from 
0.015 to 0.025 mm. long, with a cluster of flagella at one end and 

1 Consult Stroebe, Central, f. allg. Path, und Path. Anat., Bd. v., pp. 63, 67, 
1894. 

11 



130 PARASITES. 

an undulating membrane, frequently mistaken for cilia, upon the 
side (Fig. 34). It is of occasional occurrence in vaginal exudates. 

Trichomonas has been found in the urine of men, in the intestines, 
and in the sputum. Its pathogenic power is not yet defmiteh T deter- 
mined. 1 

The possibility of mistaking the T. vaginalis for human sperma- 
tozoa should be borne in mind in medico-legal examinations, although 
to an observer familiar with either structure such a mistake could 
hardly occur. 

The protozoa may be studied in the living condition either in the fluids in which 
they are found or in three-quarter-per-cent salt solution. They may be killed and 
preserved by allowing a drop of one-per-cent osmic acid to run under the cover 
glass, and replacing this after an hour by glycerin lightly tinged with eosin. Or 
they may be killed and preserved in sublimate solution. 

Many of the smaller forms show well when dried on the cover glass and stained 
by the anilin dyes by the methods used for bacteria (see page 154) . 

The movements of the Amoeba coli may be studied on the warm stage in the faeces 
or in the contents of abscesses which frequently contain them in enormous numbers, 
in three-quarter-per-cent salt solution. Its morphology may be studied in tissue 
containing them, such as intestinal ulcers, abscesses, etc., which have been hardened 
in alcohol and stained either with methylen blue or hematoxylin, the former being 
especially commended by Councilman and Lafleur. 

WORMS. 

Trematoda (Flukes). — These worms are small, flat, tongue- 
shaped or leaf -like creatures, with an intestine, and discoidal struc- 




Fig. 35.— Distoma hepaticum. About natural size. 

tures on the under surface, by means of which they attach them- 
selves. There are several genera and species found in man. The 
most common genus is Distoma, Of these D. hepaticum is of most 
frequent occurrence (Fig. 35). 

It is about 30 mm. long, and usually occurs in the gall ducts and 
gall bladder. The embryos are attached generally to water plants, 
from eating which the infection is believed to oscur. D. lanceola- 
tum is more slender, pointed at the ends, 8 to 10 mm. long, and has 
been found a few times in the gall bladder. D. sinense is a slender 
worm about 15 mm. long, and has been found in the bile in consid- 
erable numbers, particularly in the Chinese. D. haematobium is a 

1 For important original observations on Trichomonas with an historical sum- 
mary and literature see Dock, "Trichomonas as a Parasite of Man. " The American 
Journal of the Medical Sciences, vol. cxi., p. 1, 1896. 



PARASITES. 



131 



more nearly cylindrical worm ; the sexes are distinct ; the male from 
12 to 14 mm. long, the female 16 to 18 mm. long, and occurs, espe- 
cially in Egyptians, in the portal and other abdominal veins. 

Cestoda (Tape Worms). — These important worms consist, in the 
mature state, of more or less rectangular or elongated segments, 
each one of which represents a single individual, arranged in a linear 
series to form a colony, at one end of which, called the head, is a 
variously formed structure for the^ attachment of the colony to its 
host. The neck and head are called the scolex, while the segments 
are called proglottides. These worms have neither mouth nor ali- 
mentary canal. They are hermaphrodites, the sexes being united 




W 




Fig. 36. Fig. 37. 

Fig. 36-— Head of T^nia solium, x about 40. 
Fig. 37.— Head and Proglottides of T^nia mediocan-ellata. 

A, head, x about 15. 

B, mature proglottid, showing generative apparatus. 

C, head and fragments of immature proglottides, showing gradual tapering of the neck. 
Natural size. 

in the proglottides. The head and neck (scolex) may exist as an 
immature form in various tissues and organs where they are en- 
cysted, and are often called cysticercus. 

Tcenia solium is of frequent occurrence in man. It may be 
several metres in length, and may be coiled up or stretched out in 
the small intestines. Several worms may be in the gut at one time. 
The head, about the size of a pin's head (Fig. 36), has a projecting 



132 PARASITES. 

proboscis or rostellum, around which are arranged a double row of 
horny hooklets. Below these are four sucking discs at the sides of 
the head. The hooklets of the anterior row are larger than those in 
the posterior row, and are from 0.16 to 0.18 mm. long. The proglot- 
tides, when fully developed, are from 10 to 12 mm. long and from 5 
to 6 mm. wide, but those nearest the head are much shorter and im- 
mature. The eggs of T. solium are ovoidal structures, about 0.03 
mm. in diameter. The embryo of this worm is most commonly seen 
in the muscles of the pig as an encysted scolex, commonly called a 
" measle." It occasionally occurs in man in the muscles, brain, eye, 
etc., and is called cysticercus cellulosce. It is usually about the 
size of a pea, but may be as large as a pigeon's egg and surrounded 
by a connective-tissue capsule. 

Infection with the worm occurs in the human subject from the 
ingestion of insufficiently cooked " measly " pork, or, in the case of 
cysticercus cellulosse, from the ingestion of the eggs, which may, in 
a variety of ways in uncleanly persons, get into the food. 

Taenia mediocanellata (T. saginata Leuckart). — The head of 
this species is somewhat cuboidal, without either rostellum or hook- 
lets, but with four sucking discs (Fig. 37). The segments are gen- 
erally broader and shorter than in T. solium, and the worm is usually 
larger. In the embryonal form the scolex occurs as the Cysticercus 
tcenice mediocanellatce in the form of small cysts in the muscles of 
cattle, from the eating of which in the uncooked condition the infec- 
tion occurs. This is the most common tapeworm in the United 
States. 

Taenia echinococcus. — This worm in the mature condition 
forms a short, small colony inhabiting the intestine of the dog. 
The head is about 0.3 mm. in diameter and has a double row of 
hooklets around the rostellum. The proglottides are three or four 
in number, the last being the larger. The entire colony is not more 
than 4 to 5 mm. in length. The significance of this parasite in hu- 
man pathology depends upon the cysts, called hydatids, which it 
forms, in the immature or cysticercus stage, in various parts of the 
body. Intimate association with dogs favors the acquirement of this 
parasite. When the eggs of the mature worm get into the intestinal 
canal of man they undergo partial development and find their way 
into the tissues and organs, most frequently into the liver. Here 
cysts are formed which become encapsulated by a connective-tissue 
membrane produced by the inflammatory reaction of the organ. 

The cyst wall of the parasite is formed of two layers — an outer, 
finely lamellated layer called the cuticula (Fig. 38), and an inner, 
granular layer, containing muscle fibres and blood vessels, called the 
parenchymatous layer. Inside of the primary cyst secondary cysts 



PARASITES 



133 



sometimes form, called daughter cysts, and within the latter tertiary 
cysts, called granddaughter cysts, may develop. On the inner sur- 
face of the cysts, either primary, secondary, or tertiary, the scolices 
or heads of the immature worm are formed. These develop in the 
walls of the pediculated vesicles called brood capsules. The walls 
of these vesicles have a lamellated cuticula and a parenchymatous 
layer similar to those of the primary cysts. The scolices, of which 




Fig. 38.— Cuticula of Echinococcus Cyst. 
Showing lamellated structure. 



there may be several in each brood capsule, are similar to the heads 
of the mature tapeworm. They are about 0. 3 mm. in diameter, hav- 
ing a rostellum surrounded by a double row of hooklets and four 
sucking discs. At the posterior end of the scolex is a pedicle by which 







Fig. 39.— Scolices of T^inia echinococcus, x 60. 
In one the rostellum is projected, in the others it is withdrawn. 



it is originally attached to the wall of the brood capsule (Fig. 39). 
Little, lamellated concretions of lime salts are often present in the sco- 
lex. The anterior portion of the scolex, the rostellum, hooklets, and 
suckers, are often invaginated in the posterior portion. The scolices 
may be free inside of the brood capsules, or, owing to the rupture of 
the latter, they "-may be free in the cavity of the primary cysts. They 
may die and degenerate, forming a granular mass in which the hook- 



134 PARASITES. 

lets may be embedded, or the hooklets may be free in the brood cap- 
sules or in the primary cysts. Sterile cysts are often found, that is, 
those in which neither brood capsules nor scolices are developed. 

The cysts contain, in addition to the scolices, a clear, gelatinous 
fluid. This fluid may become turbid by admixture with disinte- 
grated scolices or fragments of the parenchymatous layer, or it may 
contain fatty detritus, cholesterin crystals, and particles of lime salts. 
The fluid may be partially absorbed, leaving a thick, grumous mate- 
rial within the cysts, which may become calcified or converted into a 
stony mass. When the scolices are not found entire the diagnosis 
may be made by the discovery of the separate hooklets (Fig. 40) or 
fragments of the characteristically lamellated cyst walls. The con- 
nective-tissue walls of the primary cysts may become fatty or cheesy 
or calcified. 

Sometimes the secondary vesicles project outward instead of in- 
ward, forming a series of cysts outside of the primary one. This va- 




Fig. 40.— Hooklets from Scolex of Taenia echinococcus. 

riety of development is sometimes seen in man, but is more common 
in the domestic animals. It is called Echinoccocus scolecipariens 
or exogena. 

Another variety of echinococcus, called E. multilocularis, is 
almost always found in the liver, and appears to be the result of in- 
complete and disturbed development of the embryos or cysts. It con- 
sists of a congeries of irregular, usually small cysts, surrounded by 
broad and narrow bands of connective tissue, and sometimes contain- 
ing gelatinous fluid and scolices or hooklets ; but the latter struc- 
tures are commonly absent or difficult of detection. The whole is 
often surrounded by a dense connective-tissue capsule which may be 
calcified. The entire mass often presents an alveolar structure and 
was formerly regarded as a tumor — alveolar cancer. The diagnosis 
may be established by the discovery of the hooklets or scolices, or 
fragments of the lamellated cuticula (see page 109). 

There are four or five other species of taenia, occurring rarely in 
man. 



PARASITES. 



135 



Taenia nana. — This species occurs in the form of small colonies, 
about 15 mm. in length. The rostellum is surrounded by a single 
row of hooklets. It has been seen once in large numbers by Bilharz 
in the duodenum of a child which died of meningitis in Cairo. 

Taznia flavopunctata, a species about which little is known, is 
reported twice in America as occurring in the intestine of young 
children. 

Taenia madagascariensis, also little known and rare, has been 
seen in two children in Madagascar. 

Taenia cucumerina. — This species occurs in colonies about 20 
cm. long. The head is very small and spheroidal, and has four rows 
of hooklets. It is frequent in the small intestines of dogs or cats. 
It occurs occasionally in man. Its scolex inhabits the dog louse, and 
infection may occur in man by the transference of the lice or the em- 
bryos of the parasite to the mouth, as the result of the filthy habit of 
kissing dogs and cats or permitting the face to be licked by them. 

Bothriocephalus latus. — This, the largest of the human tape- 




Fig. 41.— Ascaris lumbricoides. About half natural size. 
A, Male. B, Female. After Perls. 

worms, has very broad, quadrangular proglottides. The head is 
ovoidal and about 2 mm. long and 1 mm. broad. It has no proper 
sucking discs and no hooklets, but by long grooves on either side of 
the head the animal attaches itself to its host. The neck is long and 
filiform. It occurs most frequently in Europe, particularly in the 
northern provinces. The eggs undergo partial development in water, 
and are taken up by the pike and eel-pout, and perhaps by other 
fresh- water fish, from the ingestion of whose flesh in an imperfectly 
cooked condition the human infection occurs. Two other species of 
Bothriocephalus have been described as of rare occurrence in man : 
B. cordatus in Greenland and Iceland, and B. cristatus. 

Nematoda (Round Worms). — These worms are in general cylin- 
drical, elongated, usually pointed at the ends, and sometimes fili- 
form. The surface is sometimes smooth, sometimes irregularly beset 
with hairs and papillae, or possesses longitudinal elevated striae or 
transverse rings ; but the body is not segmented. There is a mouth 
at the anterior portion, and a ventral anus near the posterior end. 
The intestine is -straight. The sexes are in most forms distinct, the 
male being in general smaller than the female. 



136 PARASITES. 

Ascaris lumbricoides. — This is one of the most common of the 
human intestinal parasites, and is of particularly frequent occurrence 
in children. It is of a light-brownish or reddish color. The female 
is from 30 to 40 cm. long and from 5 to 6 mm. thick. The male is 
somewhat more than half as large (Fig. 41). Both sexes are pointed 
at the ends, the posterior end of the male being curved into a spined 
hook. The eggs, from 0. 05 to 0. 06 mm. in diameter, are surrounded by 
an albuminous envelope (Fig. 43) and are quite resistant to destructive 
agencies. The mode of development and life history of these parasites 
are not very well understood. Their usual seat in man is the small 
intestine, but they may wander into the stomach, and exceptionally 
get into the mouth, nose, bronchi, gall passages, peritoneal cavity, 
etc. They may be single in the gut or present in great numbers. 

Two other species of ascaris have been found in man. A. mari- 



Fig. 42.— Oxyuris vermicularis. 
A, Female. B, Male. 

timet, was found in the vomit of a child in Greenland, in an immature 
condition. A. mystax, a tolerably common form in cats and dogs, 
has been found a few times in man. It is smaller than A. lumbri- 
coides. 

Oxyuris vermicularis {Threadworm or Pinworm). — This spe- 
cies is very small ; the female has a pointed tail and is about 1 
cm. long. The posterior end of the male, which is about 4 mm. 
long, is blunt, and after death somewhat curled (Fig. 42). The eggs 
(Fig. 43) are produced in great numbers, are oval, and about 0.052 
mm. long. This parasite is very common in children, and may be 
present in large numbers in the colon. They may, in the female, 
enter the vagina and uterus. This worm is only known to infest the 
human subject, and infection doubtless occurs by the ingestion of the 
eggs, which are widely distributed in a variety of ways on many 
objects, fruits, etc. 

Strongylus gigas. — This is a slender red worm, the female being 
sometimes 1 metre long and over 1 cm. in diameter. It has been 



PARASITES. 



137 



found several times in the pelvis of the kidney in man. It is more 
common in the wolf, fox, horse, seal, and some other animals. 
Strongijlus longevaginatus.— The female is about 2.5 cm. long, the 
male, as usual, shorter. It is of a yellowish- white color, and has 
been found once in the lung of a boy in Germany. 





A 

Fig. 43.— Eggs of Nematode Worms. 
A, eggs of Ascaris lumbricoides, x about 300. B, eggs of Oxyuris vermicularis, x about 250. 



Strongylus subtilis. — A very small species (female 5.6-7 mm. 
long) has been described by Loos as occurring in Egypt in the human 
intestine. But it is believed to be without pathological significance. 




Fig. 44.— Trichocephalus dispar. 
From the skin of the mons veneris. 



Dochmius duodenalis. — The female is from 1 to 2 cm. long, the 
male about 1 cm. long. The body of the male is dilated anteriorly 
and curved backward. Its mouth is furnished with a chitinous cap- 
sule and chitinous claws and teeth. It is found in the small intes- 
tine of man in Italy, Switzerland, Egypt, and Brazil. The head is 
burrowed into the mucous membrane of the host, and the animal is 
nourished by the blood which it sucks out, and which is usually seen 
in its intestine. An ecchymosis is produced at the point of attach- 
ment, or even severe haemorrhage, and marked anaemia may be the 
result of the presence of large numbers of the parasites. 

Trichocephalus dispar (Whipworm). — The males and females 
are of nearly equal size, 4 to 5 cm. long. A little less than one-half 
of the body (the posterior portion) is about 1 mm. thick, and in the 
12 



138 PARASITES. 

male is rolled into a flattened spiral, but in the female is but slightly 
bent. The anterior part of the body is very slender (Fig. 44) and is 
embedded in the mucous membrane of the host. The eggs are elon- 
gated, oval-shaped, about 0.05 mm. long and about one-half as wide, 
with a thick brown capsule. This parasite is very common in some 
countries, especially in France and southern Italy. It is commonly 
found in the caecum, usually in small, but sometimes in very large, 
numbers. A specimen was found by Brockway in a case reported 
to the New York Pathological Society, January, 1892, with the head 
embedded in the subcutaneous tissue of the mons veneris in a dis- 
secting-room subject of unknown history. It is usually of little 
pathological significance, commonly producing no symptoms. Its 
developmental history is not well known. 

Trichina spiralis. — The female of this most dangerous and com- 
mon parasite is, in the mature condition, about 3 mm. long, the male 
from 1 to 1.5 mm. long; they are filiform in shape and white in 
color. The young are born in the form of tiny worms about 0.01 
mm. in length and somewhat similar to the adult in shape. Infec- 
tion occurs in man from the ingestion of insufficiently cooked pork. 
The muscle of the diseased pig contains the embryos of the parasite 
in an encysted condition. In the stomach the capsule of the worm is 
dissolved and the embryos are set free. They very rapidly mature, 
increasing in size, and the females give birth in the small intestine 
to very large numbers of young. It is estimated that a single fe- 
male may give birth to from 1,300 to 1,500 young. These find their 
way, through the mucous membrane and wall of the gut, into various 
parts of the body. 

The exact course which they take in getting out of the gut is not 
fully established ; probably they traverse the tissues in different 
ways. At any rate, they find their way to the voluntary striated 
muscle tissue, which they penetrate, and enter the muscle fibres. 
Here they cause a disintegration of the contractile substance, and 
coil themselves inside of the sarcolemma. In this situation they be- 
come encapsulated by material in part furnished by themselves, in 
part by means of the inflammatory reaction which their presence in- 
duces in the connective tissue of the muscle. The worms are sur- 
rounded inside the capsule by granular material (Fig. 45). The 
capsule after a time becomes partially calcified, and in this condition 
may be readily seen by the naked eye as a tiny white speck. In this 
encysted state they may remain inactive but living for an indefinite, 
often for a very long time. Most frequently the cysts contain but 
one embryo, but they may contain from two to four. The embryo 
may die and its remains become calcified. 



PARASITES. 139 

The same course of events transpires when the muscle trichinae 
are eaten by the pig or a variety of other animals. 

The embryos in the muscle are killed by a temperature of 55° C. 
and by some of the methods of curing pork. 

The embryos may mature and a new generation be born within 
from five to eight days after the ingestion of the diseased meat. 

As the result of the presence of these parasites in the body, if 
the invasion be severe, acute catarrhal enteritis, with diarrhoea and 
vomiting, high fever, and severe pains, is apt to occur. (Edema of 
the face and of other parts of the body, broncho-pneumonia, and fatty 
degeneration of the liver may be found at the post-mortem examina- 
tion of cases which have succumbed to the disease. The encapsu- 
lated embryos may be found in enormous numbers in various volun- 
tary muscles of the body, but they are most apt to be found, when 





V_. ! 



■m 



Fig. 45. — Trichtn^; encysted ts Muscle. 
In one capsule the parasite is dead and its remains calcified. 

not very abundant, in the muscles of the neck and larynx, in the 
intercostals and the diaphragm. They tend to collect toward the 
tendinous extremities of the muscles. Trichinae also occur in the 
rat, cat, mouse, and other animals. 1 

1 For the examination of muscles for the detection of the presence of the parasite, 
small pieces are snipped out with the scissors, and squeezed into a thin sheet between 
two slides, and examined with a low power. A considerable number of bits of 
muscle should be examined, particularly from the above mentioned favorite situa- 
tions, before excluding them in a suspected case, because they are sometimes pre- 
sent in small numbers. A thorough search is of especial importance in the examina- 
tion of pork, since, owing to the enormous fertility of the parasites, even a moderate 
number may give rise to a severe infection. 

For the minute examination of the parasite, bits of muscle should be hardened in 
Muller's fluid and alcohol, and decalcified if necessary, and, after embedding in cel- 
loidin. thin sections cut and stained double with hematoxylin and eosin, and mounted 



140 PARASITES. 

Filaria medinenis (Guinea worm).— This is a thread-like worm ; 
the female, which is alone known, being sometimes as much as 80 
cm. long and from 0.5 to 1.7 mm. thick. It is common in the East, 
and inhabits the subcutaneous connective tissue, in which it often 
gives rise to abscesses and ulcers. The embryos live for a time free in 
fresh water, and are then taken up by a species of fresh-water crusta- 
cean, in whose body they undergo further development, and by the 
ingestion of which the infection of the human subject occurs. 

Filaria sanguinis hominis.— The embryo of this parasite, which 
inhabits the blood and lymph of man, especially in Brazil, Egypt, 
and some parts of the Orient, and occasionally occurs in this coun- 
try, is about 0.35 mm. long, rounded anteriorly, and pointed at the 
tail (Fig. 46). It has about the diameter of a red blood cell. It 
occurs, sometimes in great numbers, in the blood during the night 
time, being as a rule absent during the day. It may occur in the 




Fig. 46.— Filaria Sanguinis Hominis. 
From a case in the New York Hospital. The specimen was prepared and loaned to the writer 
by Dr. F. Ferguson. 

urine in connection with chyluria and hsematuria. The mature fe- 
male is from 8 to 10 cm. long, and has been found inhabiting the 
lymph vessels of man, particularly in the scrotum and lower ex- 
tremities. Owing to the obstructions which it causes in the lymph 
circulation, and to the local irritation which its presence induces, it 
sometimes gives rise to lymphangiectasis, oedema, abscesses, and 
perhaps elephantiasis. One of the embryonic stages of develop- 
ment is believed to transpire in the body of a species of nocturnal 
mosquito. Through the bodies of the dead mosquitoes, which are 
liable to fall into the drinking water, it is believed that the spread of 
the parasite may occur. 

There are several other species of filaria occasionally found in 
man which it is not necessary to enumerate here. 

Ehabdonema strongyloides. — A small, filiform worm from 1 to 

in balsam. Bits of muscle may be also teased, the embryos picked out with a needle, 
and the cysts either broken open under a lens with the needle, or squeezed under the 
cover glass. The embryo worm thus set free may be mounted in a mixture of equal 
parts of glycerin and picric acid. The adult forms, which may be obtained by feed- 
ing rabbits with uncooked trichinous muscle, and examining after the proper in- 
terval, may be hardened in Muller's fluid, and mounted in a mixture of equal parts 
of picric acid and glycerin., or in the same mixture which has been lightly tinged 
with eosin. 



PARASITES. 



141 



2 mm. in length is found, often in enormous numbers, in the intes- 
tines, biliary and pancreatic ducts of man in Cochin China and in 
Italy, giving rise to endemic chronic diarrhoea. It has been thought 
that there are at least two species, which have been described under 
the generic name Aguillula, but recent researches by Leuckart 
have led him to believe them to be different developmental stages of 
the same form, for which he suggests the above name. 

ARTHROPODS. 

The scope of this work does not permit us to enter in detail into 
the subject of external parasites, which will be found described in 
treatises on diseases of the skin or in the general works on parasites 





Fig. 47. 
Fig. 47.— Sarcoptes Hominis— the "itch insect.' 1 
Fig 48. — Pediculus Capitis— the " head louse. 1 ' 



Fig. 48. 
Female; back view. After Furstenberg. 
Male. After Braun. 



referred to below. But, owing to their frequent occurrence and 
practical importance, we may briefly describe two of the more com- 
mon forms of arthropods, the "itch insect" and the " louse." 

The common "itch insect "Sarcoptes hominis (Acarus sca- 
{ e i)—is shaped somewhat like a turtle, with a chitinous covering, 
and presents the general appearance seen in Fig. 47. The female is 
about 0.45 mm. long, the male a little smaller. 

The parasite bores little tunnels in the skin, in which the eggs are 
laid and the young hatched. After a few days these bore fresh 
channels in the skin. For their detection a bit of the superficial 
layer of the skin is snipped out with curved scissors, dehydrated and 
cleared up with oil of cloves, and examined under a low power, when 
the tunnels and. the parasites, if present, will be readily visible. 

The head louse, Pediculus capitis, is from 1 to 2 mm. long, the 



142 PARASITES. 

female being slightly the larger. The general appearance of the in- 
sect is seen in Fig. 48. 

MODES OF STUDY AND PREPARATION OF THE ANIMAL PARASITES. 

The methods of studying the protozoa have been given above. 

The smaller and embryonic forms of the various kinds of para- 
sitic worms may be hardened, best under the cover glass, with 
Muller's fluid or osmic acid, and these may be, when the hardening 
is completed, replaced by dilute, and this by strong alcohol, and the 
latter finally replaced by eosin-glycerin, in which the specimens are 
permanently preserved ; or they may be stained lightly by tinging the 
alcohol with eosin, and then cleared up by oil of cloves, and finally 
mounted in balsam. 

It is necessary, however, for detailed study of the larger para- 
sites, to make thin longitudinal and transverse sections from dif- 
ferent parts of the body. This can be readily done, even in very 
small forms, by embedding the animal — after careful hardening in 
osmic acid or in Muller's fluid, and afterward in alcohol — in cel- 
loidin or paraffin, and using the microtome. The sections may be 
stained double with hematoxylin and eosin, and mounted in balsam. 

The general arrangement of the generative organs in the proglot- 
tides of tapeworms may be well seen by staining in eosin or eosin- 
glycerin after moderate hardening in dilute alcohol, and then 
squeezing the segment between two glass slides. The itch insect 
and louse may be soaked for a few hours in turpentine and mounted 
in balsam. 1 

1 Bibliography. — Especially to be recommended for detailed description of human 
animal parasites, together with practical suggestions for their study, is the small 
work of Braun, "Die thierischen Parasiten des Menschen," 1888, which contains 
also the more important older bibliography. 

The more extended classical works of Cobbold, " Entozoa of Men and Animals,'* 
1879, and Kuchenmeister and Zurn, " Die Parasiten des Menschen," 2d ed., and the 
work of Leuckart, "Die menschlichen Parasiten," should be consulted, and contain 
valuable bibliography. Various forms of external parasites of men and animals are 
fully described and illustrated in the work of Megnin, ' * Les parasites et les maladies 
parasitaires chez l'homme," etc., 1880. The plates of Stein, illustrating the Cestoda, 
1882, are carefully executed. In the " Report on Trichinae and Trichinosis, " in 1880, 
by Glazier, Surgeon in the Marine Hospital Service, will be found an illustrated ac- 
count of the natural history of this parasite, history of the disease, etc., and a section, 
on its occurrence in the United States. 



VEGETABLE PARASITES, 

The vegetable parasites of man belong among the lowly plants, 
three distinct forms of which are of frequent occurrence in or upon 
the body. These are: 

1. Bacteria, or fission fungi (Schizomycetes) . 

2. Yeasts, or yeast fungi, or sprouting fungi (Saccharomycetes). 

3. Moulds, or mould fungi (Hyphomycetes). 

The first group, the bacteria, is of the greatest significance, be- 
cause it contains organisms which are very frequently the cause of 
serious disease. 1 

I. BACTERIA. 

Bacteria are minute unicellular plants devoid of chlorophyll, mul- 
tiplying by transverse fission and in some cases by means of spores. 

The colorless, sometimes granular, protoplasm is enclosed by a 
membrane, and some forms are surrounded by a transparent capsule. 
Not infrequently parts of the protoplasm appear less dense than the 



^vv 



•* v 




Ftg. 49.— Drawtng of Three Typical Forms of Bacteria Illustrating the Three Classes. 
Stained with fuchsin. 

rest, as if from vacuolation, and a few observers have claimed to 
demonstrate in certain forms a nuclear structure. But owing to their 
minuteness, studies of the structure of the protoplasm of bacteria have 
thus far led to but meagre results. 

The various forms of bacteria may be grouped into three classes. 

1 The term micro-organism includes all of these forms of minute and lowly plants. 
They are also sometimes spoken of collectively as germs. 



144 VEGETABLE PARASITES. 

1. Spheroidal bacteria-cocci or micrococci (singular, coccus, 1 
micrococcus). 

2. Rod-like bacteria-bacilli (singular, bacillus). 

3. Spiral bacteria-spirilla (singular, spirillum). 

All straight bacteria which have one axis longer than the other 
are called bacilli, even though the form is oval rather than rod-like. 
The ends of bacilli may be square or rounded. 

While the cocci elongate a little in preparation for fission and in 
this condition present a slight irregularity in the length of their axes, 
and thus resemble bacilli, the complete observation of their life cycle 
rarely permits error in the determination of the primary group to 
which a given micro-organism belongs. 

Some bacteria present slight modifications of the fundamental 
form in certain phases of their growth. Thus some of the cocci 
after division are slightly flattened on their contiguous sides ; certain 
bacilli may bulge slightly in the middle — Clostridium forms ; others 




Fig. 50. — Bacilli showing Flagella. 

may be larger at one end than at the other — racket-shaped; some 
bacilli present considerable irregularities among individuals from the 
same growth in breadth and size and length. But these slight varia- 
tions in form rarely give rise to serious difficulty in classification. 

Finally, when bacteria are placed under conditions unfavorable for 
the maintenance of their life processes, and when they are dead, they 
are often irregularly swollen and contorted or may undergo partial 
disintegration, giving rise to what are known as " involution forms. " 

While all bacteria are minute there is among them considerable 
diversity in size, some being many times larger than others. 2 

Many of the bacteria, especially the bacilli and spirilla, less fre- 
quently the cocci, are furnished with hair-like processes called flagella. 

1 Pronounced kok'-us, plural kok! -si. 

2 For convenience of expression microscopists have agreed to let the letter // 
stand for the word micromillimetre, which is one-thousandth part of a millimetre. 
This unit of measure, equal to about one -twenty -five thousandth of an inch, is Often 
called a micron. 



VEGETABLE PARASITES. 145 

(Fig. 50), which are single or in tufts, and are apparently organs of 
locomotion. 

When the bacteria are about to multiply by fission thej' elongate, 
a partition line develops, they become constricted at a right angle to 
the axis of elongation, and finally two independent organisms are 
formed. 

The multiplication of bacteria by fission may, when the conditions 



VK ft 



Fig. 51.— Growth Aggregates op Bacteria. 
1, Diplococcus; 2, streptococcus; 3. merismopedia; 4, diplobacillus ; 5, streptobacilli; 6, curved 
bacilli forming spiral chains. 

are favorable, occurs so rapidly as to give rise within a few hours to 
an enormous number of new individuals. 

In many cases, the new individuals thus developed fall apart in 
a form identical with that of the parent cell. In some species, on the 




Fig. 52.— Leptothrix Buccalis with Micrococcus Colonies. 
From the mouth of a healthy person. 

other hand, the new-formed individuals are prone to cling together 
with greater or less tenacity, thus giving rise to growth aggregates 
which are more or less characteristic (Fig. 51). Thus among the 
cocci there are those in which a large part of the new individuals 
cling together in pairs. These forms are called diplococci. In others 
the pairs cling together in longer aggregates or chains. Such are 
-called streptococci. 



146 VEGETABLE PARASITES. 

A similar occurrence in the bacilli gives rise to diplobacilli and 
streptobacilli. Some of the spiral forms are due to the close junc- 
tion end to end of oppositely curved segments. Certain long thread- 
like micro-organisms closely allied to the bacteria are called lepto- 
thrix. 

Certain cocci divide in two directions at right angles to each 
other, giving rise to four cocci clinging together and lying in the 
same plane. These are called merismopedia forms. 




Fig. 53.— Sarcina. 
Showing growth aggregates in cuboidal masses. 



Finally cocci may divide along three planes at right angles to 
each other, giving rise to cuboidal packets of eight germs or some 
multiple of this — such growth groups are called Sarcina 1 (Fig. 53). 

There are a few branching or filamentous forms of micro- 
organisms closely allied to, if not wholly characteristic of, the bacteria 




Fig. 54.— Bacteria with Capsule. 

called cladothrix, crenothrix, and beggiotoa, which may be merely 
mentioned here. 

Actinomyces, also closely related to the bacteria, will be con- 
sidered in another section of this book. Many bacteria are surrounded 
by a broad homogeneous envelope called the capsule (Fig. 54). 

Their apparently simple structure and the lowly position which, 
bacteria occupy in the scale of living things have given rise to the 
conjecture that marked changes in form within the limits of the 
primary groups, or even changes from one primary group to another, 

1 Bacteria in masses embedded in and held together by a more or less abundant 
homogeneous material which they elaborate are called zooglcea. 



VEGETABLE PARASITES. 147 

might be brought about by alterations in environment, food, etc. In 
the early days of the exact study of bacteria this belief in pleo- 
morphism in bacteria found ready currency. 

But the more exact study of separate forms which the new tech- 
nique has made possible has led to the general acceptance of the 
view that variations do not occur except within comparatively narrow 
limits, and that what we are accustomed to call species of bacteria 
maintain their morphological characteristics with tenacity under the 
most varied changes in environment, even though these persist 
through the countless generations which may pass within the limits 
of a single experiment. 

The physiological characters of bacteria are, as we shall presently 
see, subject to wide aud significant alterations, but so far as we can 
now see monomorphism widely if not exclusively prevails. 

Under a variety of conditions, the limitations of which are not. 
very well understood, new bacteria are produced, and the species is 
perpetuated, not by simple division, but by the development of 

m % 



Fie. 55.— Bacilli showing Spores. 
The bodies of the bacilli are stained with methylen blue, the spores with fuchsin. 

spores. The most common mode of spore formation is called endog- 
enous. A small, shining mass makes its appearance within the 
protoplasm from which it is formed, grows more and more distinct, 
and finally appears as a sharply defined spheroidal or oval, strongly 
refractile colorless body (Fig. 55), which can be separately stained 
and may remain within the old cell membrane or may free itself by 
rupture of the latter. Only one spore develops in a single germ. 
Endogenous spore formation is common in bacilli, rare in spirilla, 
unknown in cocci. The spores appear to be surrounded by a dense 
envelope, and are, as a rule, much more resistant to deleterious 
agencies, such as heat, drying, etc., than are the negative forms of 
the bacteria themselves. 

Vacuoles in bacteria are often mistaken for spores. Spores, when 
placed under favorable conditions in the presence of moisture and 
nutriment, swell, become less refractile, and develop into the usual 
vegetative form. Another mode of sporulation — arthrogenous — has 
been described,' but its nature is not well understood, and even its- 
occurrence is doubted by many. 



148 VEGETABLE PARASITES. 

The bacteria require for their nutrition carbon, hydrogen, oxygen, 
and nitrogen, and certain mineral salts. All of these they can obtain 
from albuminoids and carbohydrates. Free oxygen is necessary for 
the growth and activities of some forms of bacteria and for others 
not. 

Those bacteria which require free oxygen are called aerobic. 
Those which do not grow in its presence are called anaerobic. But 
between these extremes there are forms which make shift to grow 
without oxygen under favorable conditions, though they make use of 
it when present; others grow in its presence, though flourishing best 
in its absence: these are called facultative aerobes or facultative 
anaerobes, in distinction from those first mentioned, which we call 
obligate aerobes or anaerobes. 

Nitrogen may be obtained by some bacteria from inorganic salts 
of ammonia, from nitrites and nitrates. 

Bacteria are active only in the presence of moisture; but when 
this and other conditions favoring their activity fail they do not 
necessarily die, but some forms may remain, either as spores or as 
fully developed organisms, for long periods wholly dry and inert, 
but capable of resuming their activity whenever they are again 
restored to favorable conditions. 

They grow best, as a rule, when in an organic food medium 
which is neutral or slightly alkaline. 

Some bacteria are and some are not very sensitive to changes of 
temperature. At a temperature below +5°C. they are incapable of 
marked activity or proliferation. 

At +7° C. a slow growth has been observed in various species. 
Many forms may remain alive for long periods frozen in ice, 1 while 
some are not killed by a temperature of —111° C. As the temperature 
is raised their activities increase up to a certain point. It may be 
said in general that they are most active at about the temperature of 
the bod3% although species differ considerably in this respect. In 
fluids many bacteria are killed by a prolonged exposure to a temper- 
ature of from 60° to 70° C. or even less. On the other hand, certain 
species grow at a temperature of from 60° to 75° C. Such are called 
thermophyllic bacteria. 2 

All known bacteria, save for a few very invulnerable spore-form- 
ing species, are killed by prolonged exposure in the presence of 
moisture to a temperature of 100° C. 

When dry they resist much higher temperature than when moist. 

1 Prudden, "On Bacteria in Ice, etc. " Medical Record, March 26th and April 2d, 
1887. 

2 Consult Babinoioitsch, Zeitschrift f. Hygiene u. Infectionskr. , Bd. xx. 



VEGETABLE PARASITES. 14$ 

The spores are, as a rule, more resistant to high temperatures than 
the bacteria themselves, some having been exposed, dry, to a tem- 
perature of 140° C. without destruction of life. Fluids containing the 
spores of bacteria which resist very high temperatures may be steril- 
ized by boiling for a short time, then being allowed to stand at 
ordinary temperatures for several hours, and then again boiling; this 
process being repeated several times. In this way, although the 
spores themselves are not killed by the heat, the bacteria into which, 
if the conditions be favorable, they develop during the intervals are 
killed, so that finally the medium is entirely freed from both living 
spores and adult bacteria. 

Strong light is in general inimical to the life and growth of bac- 
teria, and by direct sunlight many forms are readily killed. 

Certain disinfecting agents, when brought into contact with bac- 
teria, are capable of greatly reducing their activities or destroying 
them altogether ; but different forms differ greatly in their power of 
resisting the action of these agents. The spores of certain bacteria 
are exceedingly resistant, much more so than the bacteria them- 
selves, to the action of disinfecting agents. Among these disinfec- 
tants may be mentioned formalin, carbolic acid, and especially solu- 
tions of corrosive sublimate, which is very inimical to the life of 
most bacteria and their spores, even in extremely dilute solutions. 

Some bacteria are capable of performing rapid movements, others 
are not ; and the same form may be at one time mobile and at another 
immobile, depending upon external conditions. Movement is largely 
confined to the rod-like and spiral forms, but has been observed in the 
spheroidal. 

It has been shown that certain of the motile bacteria, when sus- 
pended in fluids, are attracted toward, or repelled from, dissolved chem- 
ical substances. This is called chemotaxis, and it is termed positive 
or negative according as the organisms are attracted or repelled. 

The bacteria play a very important role in nature in virtue of 
their power of feeding upon and pulling to pieces dead organic 
materials. A part of the new chemical compounds which are thus 
formed may be used by the bacteria for the purposes of their own 
nutrition and growth, while the rest are set free to serve, sooner or 
later, as food for other forms of plants or animals. 

In the decompositions which are brought about in nature by the 
bacteria those compounds of nitrogen and carbon dioxide are set 
free which are essential for the nutrition of the higher plants. 

Without the activities of bacteria, life could not be long main- 
tained upon the earth, since the necessary carbon, hydrogen, oxygen, 
and nitrogen would soon be permanently locked up in unavailable 
form in organized material. 



150 VEGETABLE PARASITES. 

Through the action of the various nitrifying bacteria in the soil, 
ammonia is decomposed with the formation of water and nitrous 
acid; nitrous is converted into nitric acid. 

The so-called denitrifying bacteria reduce nitrates to ammonia 
and to nitrites. In these ways, among others, water percolating 
through the soil may be purged of objectionable organic compouuds. 

A large number of complex chemical substances are elaborated 
during the growth of bacteria, their nature varying with the species 
of bacteria and the composition of their nutrient material. 

Some of the chemical compounds set free by the growing bacteria 
are bad-smelling or aromatic; some are inert and harmless sub- 
stances; some are powerful poisons, and may, when they have accu- 
mulated in the fluids where they grow, inhibit the activity and 
growth or even destroy the bacteria which have produced them. 

Fermentations and putrefactions are due to the activities of micro- 
organisms, some to bacteria, some to yeasts. 

Putrefaction is a form of fermentation in which nitrogenous com- 
pounds are decomposed by micro-organisms setting free bad-smelling 
substances. 

Bacteria which induce fermentation are called zymogenic — and 
each species induces fermentation of a special character. Some of 
these are important in the arts; some are concerned in the changes 
which food products undergo under natural or artificial conditions, 
such as the development of koumyss from milk and the common 
butyric, lactic, alcoholic, and other fermentations. 

The chemical changes which are induced by micro-organisms in 
the process of fermentation are extremely complex and little under- 
stood. 

Bacteria may develop in their metabolic activities soluble ferments 
or enzymes of various kinds resembling diastase, pepsin, trypsin, 
rennet, etc. 

Many bacteria produce pigments as they grow (chromogenic 
bacteria). This pigment may be developed in or upon the germs 
themselves or may be diffused through the surrounding media. Gas- 
producing bacteria are called aerogenic. Certain species when grow- 
ing in masses emit a phosphorescent light— photogenic bacteria. 

Certain of the basic chemical compounds resembling the vegetable 
alkaloids, which are formed by the action of bacteria in organic 
matter, are called ptomains. 1 The ptomai'ns of certain special forms 
of bacteria are believed to be of importance in inducing deleterious 
effects in many of the infectious diseases; these are called toxins. 

1 Leucomains are basic products produced in the tissues of living animals by 
cell metabolism. 



VEGETABLE PARASITES. 151 

Complex proteid bodies may be produced during the growth of bac- 
teria; these may be in part set free, in part assimilated in the bac- 
terial cell protoplasm. These proteid bodies belong in part to the 
albumins, in part to the albumoses, while some of them resemble the 
peptons. Many of them seem to be most potent factors in the induc- 
tion of the phenomena and lesions of the infectious diseases. The 
poisonous albuminous substances produced in the body by the growth 
of certain disease-producing bacteria are called toxalbumins. 

Bacteria are widely distributed in the air, in water, and in the 
superficial layers of the soil, where they may be present in enormous 
numbers. They are especially abundant among the habitations of 
man, or wherever under favorable conditions of moisture and temper- 
ature animal or vegetable substances are undergoing decay. 

They cling tenaciously to moist surfaces, but when dried, and 
especially when dried upon comminuted material, they may float in 
the air as dust. In quiet air they gradually settle with other forms 
of dust on to the horizontal surfaces, and thus in closed, still rooms the 
bacteria-laden air may over night almost wholly free itself of its liv- 
ing contaminations by a process analogous to sedimentation in water. 

This widespread transportation of bacteria as dust by moving air, 
and the spontaneous cleansing of the latter by the settlement of the 
germs, are important factors in the sanitary problems which the com- 
plex conditions of modern life present. Large numbers of mould 
spores are frequently mingled with the bacteria in dust and soil. 

While bacteria may live for long periods in the dried state in dust 
they do not in this condition multiply. But the upper three or four 
feet of the soil forms the great abiding, and when moist the breeding, 
place of the myriads of germs which are concerned in the salutary 
work of food preparation for higher plants. 

Surface waters almost always contain bacteria, which may have 
entered by aerial dust or from the wash of adjacent soil or from direct 
human or animal contamination. Many bacteria find in water favor- 
able conditions of life and flourish on what to other forms would be 
but scanty nutriment. Many pathogenic bacteria may remain alive 
for considerable periods in water, but they do not usually thrive 
there. 

The water which in many places lies in hollows of the rocks, 
bathing the deeper layers of the soil or gathered in caverns and 
recesses beneath, is called ground ivater. This under favorable con- 
ditions is almost wholly free from micro-organisms, these, through 
the complex process of filtration, germ metabolism, etc., which go 
on in the upper soil layers, having, together with inorganic contami- 
nations, been largely retained or transformed as the surface water has 
slowly sought the lower levels. It should always be borne in mind 



152 VEGETABLE PARASITES. 

that, so far as we know, with few exceptions the bacteria whose 
natural habitat is the soil or air or water are not under usual conditions 
harmful to man. On the other hand, it is germs from the bodies 
of men or animals who are the victims of infectious disease, which 
in one way or another gain access to these great reservoirs and 
sources of distribution, which render the bacterial flora of soil and air 
and water occasionally of especial direct personal significance toman. 

It will be seen from what has been said about bacteria and their 
various modes of life that some live in or upon and at the expense of 
other living beings — the hosts — these are parasites. 

Others which live and grow apart from a living host are called 
saprophytes. In either class there are forms which, through the 
capacity of adapting themselves to their environment, can maintain at 
one time a parasitic, at another a saprophytic life. Such germs are 
called respectively facultative parasites or facultative saprophytes. 
Those, on the other hand, whose life is strictly limited to the parasitic 
or saprophytic condition are called obligate parasites or saprophytes. 

Not all the bacteria which live in or upon the bodies of men and 
animals are in the stricter sense parasites. The terms messmates 
and commensals have been applied to such organisms as simply live 
with, but do not necessarily derive nutriment from, the host. 

In some cases parasitic life on the part of the micro-organism may 
contribute to the welfare of the host. This is the case in some bac- 
teria which live upon the roots of certain leguminous plants, and to 
whose nutrition they contribute by rendering atmospheric nitrogen 
directly available for the host. This condition of life is called sym- 
biosis. 

As has already been indicated, the morphological characters of 
bacteria are so little subject to permanent variation under the widest 
diversity in the conditions to which they are subject that we are 
justified in the belief in fixed species. 

But so susceptible to external conditions are the functional activi- 
ties of many species that not only is the occurrence of what may be 
called varieties within specific limits frequent under natural condi- 
tions, but more or less permanent variations may be experimentally 
produced. 

Almost all of the functional activities of bacteria upon which we 
rely as descriptive characters may be experimentally altered ; thus the 
color-producing capacity may be diminished, the peptonizing and 
fermentative activities lowered, the pathogenic powers reduced or 
exalted, and even the capacity for spore formation may be abolished. 

These more or less permanent modifications of function in bacteria 
are usually induced by artificial cultivation under adverse conditions 
of temperature and nutrition, by the presence of deleterious chemical 



VEGETABLE PARASITES. 153 

agents, antiseptics, etc., or by association with the body cells and 
juice in susceptible or insusceptible animals (see page 179). 



CLASSIFICATION OF BACTERIA. 

The beginning of the systematic study of bacteria by exact and 
reliable methods is of such recent date, they are so minute, and our 
present optical apparatus reveals so few differential morphological 
characters beyond the limits of the three primary classes already men- 
tioned, and so few withal of the many existing forms have as yet 
been studied, that a satisfactory classification or nomenclature of the 
bacteria is not yet possible. 

Outside of the limits of the primary classes we are obliged to use 
for the purposes of identification and description the results of physio- 
logical activities which the special forms of bacteria display when 
placed under diverse and usually entirely artificial conditions of food, 
temperature, and general environment. It is evident from this con- 
dition of affairs that what in our attempts at classifications we are 
wont to call genera and species, are not such in the strict sense in 
which these terms are used in other domains of biology. That which 
corresponds to the generic name in the more exact vocabularies is in 
ours usually the growth form which indicates the primary class to 
which the germ belongs, as coccus, bacillus, or spirillum, or some 
growth modification of this, as diplococcus, streptococcus, strepto- 
bacillus, and the like. To this is usually appended a more or less dis- 
tinctive specific name, which usually indicates some noteworthy phy- 
siological capacity of the germ, such as its peptonizing power, the 
pigment which it elaborates, some prominent chemical reaction which 
it initiates, some marked effect upon an artificial culture medium, its 
disease-producing power in men or animals, or some fact about its 
habitat, or the situation in which it was found. All of these and 
other heterogeneous characteristics, largely functional, which may be 
developed under natural or artificial conditions, constitute data in the 
life history of germs upon which the classification and nomenclature 
of bacteria are at present based. 

As examples of names of bacteria thus derived may be cited 
Micrococcus luteus, Diplococcus lanceolatus, Sarcina ventriculi, 
Bacillus acidi lactici, Spirillum cholerce Asiaticce. 

Notwithstanding the value of this principle of grouping and 

nomenclature, its inadequacy even for temporary use is becoming 

painfully evident as research proceeds, partly because of the large 

variations to which physiological activities are liable, and partly 

because we cannot sharply distinguish between races, varieties, and 

species. 

13 



154 VEGETABLE PARASITES. 

It is not yet possible to say whether it will ever be practicable in 
this limited field of lowly life to draw such exact distinctions between 
genera and species as the wider domains of biology permit. 

METHODS OF STUDYING BACTERIA. 

The simplest mode of studying bacteria is to examine them either 
in the fluids in which they lie or in one-half -per-cent salt solution. 
For the study of many of the phenomena of life this method is 
important. 

This may be accomplished by the examination of a thin layer of 
the fluid under a cover slip, in the usual wa} T , or a small drop may 
be placed on the cover slip and this inverted on a hollow slide so 
that the observation is made in the hanging drop. A streak of 
vaselin painted around the edge of the cover will prevent evapora- 
tion of the fluid. 

By far the most important aid in the morphological study of the 
bacteria is derived from the use of staining agents. Most of the 
bacteria are stained more or less readily by one or more of the basic 
anilin dyes. The ease with which they are colored varies consider- 
ably in different species and with the different dyes. The tissue 
elements, and a variety of other materials with which the bacteria 
may be associated, also stain more or less readily at the same time; 
but most of these part with their color more readily than do the bac- 
teria on being treated with alcohol or dilute acids. We are thus 
enabled to obtain a differentiation in color between bacteria and 
other structures. The bacteria, moreover, differ among themselves 
in respect to the tenacity with which they hold their stain in the 
presence of decolorizing agents, and upon this fact is based one of the 
important methods of distinguishing between different species. 

Among the anilin dyes more commonly employed for bacteria 
staining may be mentioned fuchsin, gentian violet, and methylen 
blue. A saturated alcoholic solution of these dyes should be kept in 
a tightly stoppered bottle, and from this the more dilute solutions 
required for staining may be prepared. For ordinary purposes one 
part of alcoholic solution of fuchsin or gentian violet, added to twenty 
parts of water, will give a staining solution of suitable strength. 
This should be prepared in small quantities as required, since it does 
not keep well and a granular precipitate is apt to form in a few days. 

Special stains and modes of staining, such as are necessary for 
some forms of bacteria — the tubercle bacillus, for example — will be 
described under the appropriate headings. We are speaking, here 
only of the general methods. 

To Stain Bacteria in Fluids. — A small drop of the fluid is 



VEGETABLE PARASITES. 155 

placed on a cover glass which is perfectly clean and free from grease; 
spread a little with a needle, and allowed to dry by evaporation in 
the air or by gentle heating, held by the edges in the fingers, high over 
a flame. The cover glass is now held with the forceps, and, speci- 
men side up, passed moderately rapidly three times through the flame 
of an alcohol lamp or a Bunsen burner. The material on the cover 
should not be burned. This heating not only fixes the contents of the 
fluid firmly on to the glass so that it will not easily soak off, but it 
renders insoluble any albuminous materials which may be mixed 
with the bacteria, and which might otherwise interfere with subse- 
quent examinations by forming granular precipitates. 

A drop of the aqueous staining fluid is now put on to the dried 
specimen on the cover glass, and if this be held in the forceps and 
tilted slightly up and down a few times so as to bring fresh portions 
of the staining fluid into contact with the bacteria, the staining will 
usually be completed in two or three minutes. The stain is now 
washed off with a jet of water from the wash bottle, and the speci- 
men is either mounted in a drop of water for temporary study, or 
the washing water is drained off and, after drying in the air, it is 
mounted directly in balsam. 

It is well to use balsam which has been softened, when this is 
necessary, with oil of cedar or xylol rather than with chloroform, 
since this is apt to decolorize the bacteria. 

If the bacteria which are to be stained are in solid masses, as 
is usually the case in pure cultures on solid media (see below), a 
small drop of distilled water should be first put on the middle of 
the cover glass, and a very minute quantity of the bacterial mass 
rubbed into it with a platinum needle and then dried and stained 
as before. 

Gram's method (see page 156) is often useful and in some cases 
almost indispensable for the differential staining of bacteria. 

Spore Staining. — For staining spores the method of Moeller is 
generally useful. 

The cover-glass preparation of the bacteria is made in the usual 
way and fixed by heat or by immersion for two minutes in absolute 
alcohol. It is then placed for one minute in a five-per-cent solution of 
chromic acid, then thoroughly rinsed in water and stained for one 
minute in a small dish of Ziehl's solution (page 224) heated to boiling. 
From this it is transferred without rinsing to five-per-cent solution 
of sulphuric acid, in which it is decolorized. The spores are now 
red, the bodies of the germs uncolored. A contrast stain of the body 
may be made with an aqueous solution of methylen blue. 

The rationale of this method is that the maceration of the spore 
membrane by chromic acid permits the penetration of the stain to the 



156 VEGETABLE PARASITES. 

spore substance. If the chromic acid act too long the subsequent 
differentiation may be impossible, owing to the too ready decoloriza- 
tion of the spore by the acid. The exact periods during which the 
various agents should be permitted to act may not be hit upon with- 
out repeated efforts with slight variations. 

Immersion of the cover slip in chloroform for two minutes is nec- 
essary after the fixation of the specimen, should fat cholesterin 
crystals or allied materials be mingled with the germs, since in the 
presence of these the differentiation of the spores is apt not to be 
clear. 

To Stain Bacteria in Tissues. — The tissues should be well hard- 
ened in alcohol. Thin sections are placed in the above-described 
aqueous coloring solutions, where they may remain from five to 
fifteen minutes. In some cases a much longer staining is necessary. 
Gentle warming (40° to 50° C.) will hasten the staining. The entire 
tissue as well as the bacteria is in this way deeply colored. The 
sections are rinsed with distilled water and then placed in alcohol. 
This, with varying degrees of rapidity with different stains and tis- 
sues, gradually extracts the color from the tissue, most slowly from the 
nuclei. The time required and the exact degree of decolorization to 
be sought for must be learned by experience in different cases. Some- 
times five, sometimes thirty minutes are required, sometimes only a 
few seconds. It is often necessary, and the decolorizing of the tissue 
is thereby hastened, to add a few drops of acetic acid to the alcohol. 
When acetic acid is used it should be finally thoroughly washed out 
by alcohol. The specimens are now cleared up by oil of cloves and 
mounted in balsam. Oil of cloves removes the color from some forms 
of bacteria, and in this case xylol or oil of bergamot should be substi- 
tuted for it. In specimens prepared in the above way, the nuclei of 
cells usually retain to some extent a color similar to that of the bac- 
teria, but their size and shape serve for the differentiation. 

Gram's Method. — This is a much more generally useful method 
of staining bacteria in the tissues than that just given, although not 
in all cases applicable. The tissues from which the sections are 
made should have been hardened and preserved in alcohol. The 
sections are stained for from two to four minutes in anilin- gentian- 
violet solution. This is prepared as follows: 1 c.c. anilin oil is 
added to 20 c.c. distilled water; this mixture is well shaken, and the 
excess of anilin oil is filtered off through a moistened paper filter. 
To the clear filtrate saturated alcoholic solution of gentian violet 
is added until the fluid becomes opalescent (about 1 part of the dye 
to 10 of the water will usually be enough). A small quantity 
only of this fluid should be prepared at once, as it does not keep very 
well. 



VEGETABLE PARASITES. 157 

From the staining solution the sections are transferred directly to 
a solution of iodin in potassium iodid and water (I 1.0 — KI 2.0 — H 2 
300.0). In this they remain from one to three minutes, a precipitate 
forming in the solution and the sections becoming of a dark-reddish 
or slate color. The sections are now transferred to absolute alcohol, 
which should be changed two or three times so as to dehydrate the 
specimen, which at the same time will lose much of its color. Final- 
ly the decolor ization is completed and the section cleared up by oil of 
cloves, and it may then be mounted in balsam. Very little of the 
violet color should be visible to the naked eye in the specimen when 
it is ready to mount. If the specimen have been embedded in cel- 
loidin for the purpose of section cutting, this will be dissolved from 
the sections by the oil of cloves. Then it is well to use a second por- 
tion of oil of cloves, so as to get rid of the superfluous half-dissolved 
celloidin. It is also well to tint the oil of cloves lightly with a few 
drops of alcoholic solution of eosin, and then the violet-colored bac- 
teria will stand out in sharp contrast with the reddish tissue elements. 
The iodin solution should never be used a second time, and a plati- 
num needle should be used in manipulating the sections, since steel 
instruments are injured by the iodin. Oil of origanum tinged with 
eosin may be used in place of oil of cloves. It does not dissolve cel- 
loidin and is thus best adapted to delicate or friable sections. 

Some bacteria are decolorized by Gram's method of differentia- 
tion. 

In this as in other methods of staining bacteria in tissue the sec- 
tions are liable to shrivel and curl. This may in many cases be 
avoided by fixing the sections on to the cover slip with albumen fix- 
ative (see page 59) before the staining begins, carrying cover glass 
as well as section through the subsequent processes. 

WeigerVs Modification of Gram's Method. — The sections are 
laid for half an hour in the anilin-gentian-violet solution prepared as 
above, then rinsed off in three-quarter-per-cent salt solution and 
spread on a slide. They are now dried with blotting-paper and 
covered for two minutes with the iodin solution. The iodin solution 
is now removed with blotting-paper and the sections decolorized with 
anilin oil or a mixture of 2 parts of anilin oil and 1 part of xylol, 
several times renewed. Finally the sections are cleared in xylol and 
mounted in balsam. 

In many cases it is well to accomplish a double staining by a pre- 
liminary contrast stain. Thus, before the use of Weigert's modifica- 
tion of Gram's stain the sections may be put for half an hour 
in a solution of picro-carmin, then rinsed in water and stained as 
above. By this modification of Gram's method fibrin is deeply 
stained. 



158 VEGETABLE PARASITES. 

Loffler's alkalin-methyl-blue solution is a very valuable and 
powerful stain for bacteria, eitber in fluids or in tissues. 
It consists of — 

Saturated alcoholic solution of Methyl Blue 30 parts. 

Aqueous solution of Caustic Potash 1 : 10, 000.. 100 " 

"For staining bateria in tissues the stain is allowed to act for a 
few minutes. The section is then put for a few seconds in one-half - 
per-cent acetic acid, then rinsed in water, and the superfluous color 
removed from the tissue by repeated rinsing in alcohol, which at the 
same time dehydrates it. Then it is cleared with oil of cedar and 
mounted in balsam. Care should be taken not to remove too much 
color with the alcohol. For staining bacteria in fluids in which there 
is little solid material other than the germs, Loffler's blue is used as 
are the ordinary simple anilin dyes, described above. 

It should always be borne in mind in staining the bacteria that 
great exactness is not usually necessary either in the strength of the 
coloring solutions or in the time of exposure of the bacteria to them. 
We are seeking for certain effects — namely, the staining of the germs 
— and this depends not only upon the quality and strength of the dye, 
the time of exposure, etc, but also upon the nature of the bacterial 
species and its conditions at the time the staining is attempted. 
Thus it not infrequently happens that bacteria which will stain 
readily and deeply with a given solution when they are in a condition 
of active growth, may scarcely be at all colored if they have been 
dead or inactive for a long time, although their outward shape 
appears to be unchanged. So it should be remembered that, while 
there is little difficulty in most cases in staining the bacteria, the 
operation is not one of mere routine, but requires intelligent attention 
to the particular conditions of the species in hand. 

The Microscope. — For the recognition and study of bacteria, es- 
pecially of the minuter forms, the best optical apparatus is requisite. 
"With good high-power dry lenses a certain amount of instructive 
observation on the bacteria may be made. But for finer study and 
research homogeneous immersion lenses (at least one-twelfth) with 
the Abbe condenser must be used. 

ARTIFICIAL CULTIVATION OF BACTERIA. 

For the complete investigation of the different forms of bacteria, 
particularly in their relations to disease, we must isolate them so as 
to be able to study their life history and the effects of their inocula- 
tion into healthy animals. It has long been known that bacteria 
could be cultivated in a variety of artificially compounded, so-called 



VEGETABLE PARASITES. 159 

nutrient media or soils. Fluids were formerly used for this purpose, 
but it is very difficult to separate single species in fluid media, and 
to detect contaminations when they occur. Moreover, the inevitable 
mechanical disturbances of the fluid prevent, for the most part, the 
formation of gross characteristic appearances in the masses of grow- 
ing bacteria. Robert Koch introduced, a few years ago, a technical 
improvement of inestimable value in suggesting and formulating the 
details of using solid media for the cultivation of bacteria. Among 
these may be mentioned sterilized boiled potatoes and gelatinized 
infusions of various natural or artificially compounded substances 
sterilized by heat. Different species of bacteria often require different 
nutrient media, and some require different temperatures for their most 
flourishing growth. They usually grow within or upon the surface 
of the solid nutrient media in sharply circumscribed masses, called col- 
onies, and different species may grow side by side in the same recept- 
acle for considerable periods without in the slightest degree interfer- 
ing with one another or tending to mix. The mode of growth and 
general appearances of the proliferating bacterial masses on the solid 
medium often present very characteristic differences between dif- 
ferent forms, and thus not only furnish valuable means of identifying 
species, but render possible an early detection of contamination from 
chance admixture of species. A given species of bacteria may be 
cultivated through a series of generations by transferring, with 
proper precautions, a minute portion from a growing colony to a 
fresh surface of sterilized soil. After cultivation through several 
generations the species may be presumed, and by microscopical 
examinations proved, to be entirely pure, and the effects, if any, 
produced by its inoculation into healthy animals, to be due to it 
alone. 

The Preparation and Use of Culture Substances.— There are 
many culture media, some of which are best suited for one, some for 
another species of bacteria. Those most commonly used are meat 
broth (bouillon), broth rendered solid by gelatin or agar-agar (called 
"nutrient gelatin" or ''nutrient agar"), boiled potatoes, coagulated 
blood serum, and milk. 

Nutrient Gelatin. — One pound of lean beef is chopped fine, 
stirred into one litre of water, covered, and set away in the refrige- 
rator for twelve hours. The red fluid is now completely separated 
from the meat by squeezing through a cloth into an enamelled sauce- 
pan, which fits into a larger vessel serving as a water bath. To the 
beef juice are added ten per cent of clear French gelatin, one per cent 
of beef pepton, and one-half per cent of common salt. The mixture 
is now heated i-n the water bath until the gelatin is dissolved, when 
it is carefully neutralized by the addition of a sufficient quantity of a 



160 



VEGETABLE PARASITES. 



dilute solution of caustic soda. It should be made exactly neutral 01 
very slightly alkaline. The reaction may be determined by litmus 
or, which is better for exact researches, by the use of a solution oi 
phenolphthalein . 

The white of two eggs well beaten is now added — to clear the 
media— -and the whole boiled vigorously for half an hour. It is ther 
filtered through a thick layer of sterilized cotton into a flask, and 
should form a perfectly clear, slightly yellowish mass which is quite 
firm and solid on cooling. It is now filled into test tubes which have 
been plugged with cotton and sterilized by heating for an hour in a 




Fig. 56. —A Tube of Solid Transparent Nutrient Gelatin. 
Showing growth of bacteria with formation of gas along the line of inoculation by a needk 
plunged into the solid gelatin and withdrawn. The bacterial masses are held fast where thej 
grow, and the gas bubbles cannot escape through the solid media, 

dry oven at 160° C. — about two inches in depth of the material being 
put into each tube — and these are steamed for twenty minutes to half 
an hour, and again for an equal period on the following day, when 
they are ready for use (see Fig. 56). 

Nutrient Agar. — This is made and filled into tubes in the same 
way as the nutrient gelatin, save that one per cent of the agar is 
added in place of the gelatin. As the agar is less readily soluble than 
the gelatin, it will have to be boiled longer on the water bath before 
neutralizing. After the last sterilization the agar tubes are placed 
in a slanting position to cool, so that the agar may present a long, 
oblique surface (see Fig. 57). 



VEGETABLE PARASITES. 



161 



The Nutrient Broth is made in the same way, save that no 
solidifying material is added and it may be filtered through paper. 

Milk. — This should stand in the ice chest for a few hours, so that 
the cream may be removed. The milk is then filled into sterile 






Fig. 57. 



Fig. 58. 



Fig. 57. —Pure Culture of Bacteria on Nutrient Agar in Sterilized Tubes. 
Showing at the left a smooth, at the right a wrinkled growth upon the surface. 

Fig. 58.— A Culture of Bacteria on Potato. In a tube plugged with cotton and 
then sterilized. 

cotton -plugged test tubes, and steamed for half an hour on three suc- 
cessive days. 

To these culture media various substances may be added which 
14 



162 EGETABLE PARASITES. 

serve to exhibit one or other functional capacity of the germ undei 
observation. Thus to the nutrient agar or gelatin litmus is some- 
times added to reveal the presence of acids, should these be developed 
in the complex metabolism of the growing germs. Sugar may be 
added to the nutrient bouillon and the culture so arranged that should 
gases be developed they may be collected, measured, and tested in a 
closed arm of the culture tube. Glycerin is frequently added to cul- 
ture media. 

Potatoes. — The potato is scrubbed with a brush under the watei 
faucet and the ends cut off with a knife, leaving a segment about an 
inch and a half long. With a tin cylinder about an inch in diam- 
eter, made like an apple corer, a cylinder is cut lengthwise out of the 
potato segment, and this is divided lengthwise with the knife intc 
two oblique sections. These pieces of potato, after lying for a few 
minutes in running water to prevent subsequent discoloration, are 
placed, the narrow end up, in large test tubes about five inches long 
and a little more than an inch wide, which have been plugged at the 
mouth with cotton and sterilized. These tubes are now steamed for 
an hour and again for an hour on the following day. 1 

Blood Serum. — The blood should be drawn from the vein at the 
slaughter house, with as little contam ination as possible, directly into 
sterile jars. When the blood has clotted, a clean glass rod maybe 
passed around the clot to free it from the sides of the jar, and the 
whole set aside for twenty-four to forty-eight hours in an ice chest. 
During this time the clot contracts and the serum is expressed. 

The clear colorless serum is then distributed with a sterile pipette 
into sterile test tubes, 4 or 5 c.c. in each tube. The serum may 
now be coagulated by heating the tubes, set aslant in a dry oven, at 
from 80° to 90° C. Then on three successive days it is steamed at 
100° C. for twenty minutes. Or, the tubes containing the fluid serum 
may be set aslant and kept for two hours at a temperature just below 
100° C. so that the serum will solidify but not boil. It is important 
for certain purposes to use human blood serum ; this may be obtained 
in small quantities from the human placenta. 

The use as culture media of pleuritic (" chest serum") and other 
transudates into the serous cavities, either alone or in association with 
agar, is important in certain lines of work. 2 

The addition to the blood serum before coagulation of one-third 
of its volume of nutrient bouillon to which ten per cent of glucose 
has been added affords a medium (Loffler's blood-serum mixture) 

1 Since the reaction of potatoes varies considerably, it is well to control this and 
secure a neutral or slightly alkaline reaction in the whole batch by soaking in dilute 
alkali before tubing and sterilization. 

2 Consult Heiman, New York Medical Record, June 22d, 1895. 



VEGETABLE PARASITES. 163 

very favorable to the growth of the diphtheria bacillus, which is much 
used in the culture method of diagnosis in that disease. 

Having thus seen how some of the nutrient media are prepared, 
let us see briefly how they are used in studying the bacteria. 

In the first place, it is necessary to get from the various mixtures 
of several species, as they are apt to occur in nature or in diseased 
parts, single species growing by themselves, so that their life history 
and characters may be studied in detail. To show by an example 
how this is done, we will suppose that we have a sample of milk 
containing bacteria, and wish to learn how many there are and of 
what species, and to get them into separate receptacles for study. 
We melt the gelatin in one of the test tubes, prepared as above 
described, which we know to contain no living bacteria — because we 




Fig. 59.— A Petri Gelatin Plate Culture of Bacteria. 
In one plate there are few colonies showing difference in size and character. In the other 
the colonies are much more abundant. (From a milk culture prepared by Dr. Freeman.) 

have sterilized both the tube and its contents by heat — and add to it 
a measured volume, usually 1 c.c, of the milk, and mix them by 
gentle shaking; we now take a shallow covered glass dish called a 
Petri plate (see Fig. 59), which has been sterilized by heat, lay it 
upon a cold surface, and pour out the mixture of water and nutrient 
gelatin in a thin layer upon it. When the gelatin solidifies, the in- 
visible germs which the milk contained are caught and held in 
position by it, and if the whole be now set away in a sufficiently 
warm place the living bacteria will presently commence to grow. 

After a few hours or days, from each one of the single living bac- 
teria scattered through the gelatin so many new germs may have de- 
veloped that they form a mass, called a colony, large enough to be 
visible to the naked eye. As different species grow in different ways, 



164 



VEGETABLE PARASITES. 



some forming colored colonies, some fluidifying the gelatin, some 
growing much more rapidly than others (see Fig. 60), we can usually 
recognize the difference in species either with the naked eye or under 
the microscope, and with a fine, sterilized platinum needle can pick 
out portions of the different colonies and transfer them to the tubes of 
nutrient media of one kind or another which we have prepared, and 
study their growth there in the form of pure cultures. 







j- 



ynP^ 



Fig. 60. — A Petri Gelatin Plate Culture op Bacteria. 

Showing colonies of various shapes and sizes ; the larger colonies are formed of bacteria of 
different species from those which form the small ones, and which were mixed together in the 
fluid (milk) originally planted in the gelatin plate. The plate is more highly magnified than in 
Fig. 59. 

The transfer of the germs to the tubes is made by plunging the 
needle which has touched the plate colonies down into the gelatin 
(Fig. 56) or agar, or drawing it over the surface of the potato. 
This is called inoculating the culture media. 

Not infrequently it is necessary to use the agar culture medium 
for plate cultures, because many disease-producing forms of germs do 



VEGETABLE PARASITES. 



1G5 



not grow at a temperature below that of the body, at which gelatin 
fluidifies. 

In many cases, especially when we make agar plate cultures, we 
•do not mix the material to be studied with the fluidified culture 
medium and then let it cool, but spread the material in very thin 
streaks, with a sterilized platinum needle, over the surface of the 
already cooled nutrient film. Then setting the culture, carefully 




Fig. 61.— Petri's Agar Plate Culture of Bacteria from the Mouth. 
Made by streaking the surface of sterilized nutrient agar— previously poured into the shallow 
dish and cooled— with scrapings from the mouth, and allowing to stand in a warm place for forty- 
eight liours. The lighter spots are the "colonies" or masses of germs of various forms which 
have grown from the invisible germs of the mouth. 



covered, in the incubator, we await the development of colonies along 
the surface streaks (see Fig. 61). 

Instead of pouring the melted nutrient gelatin or agar in which 
germs have been sown into the bottom of a flat dish, a small quantity 
of the mixture may be put into a sterilized test tube, the cotton plug 
replaced, arid the whole cooled by twirling the tube horizontally in 
cold water or upon a block of ice. 



166 VEGETABLE PARASITES. 

Thus the nutrient medium forms a thin, transparent lining to the 
tube in which subsequent colonies are readily seen. Such cultures 
are known as Esmarch roll cultures or roll tubes. 

By the use of this principle of the plate culture, sometimes with 
one form of nutrient medium, sometimes with another, and with 
various modifications of the technique, the species of bacteria can be 
separated and each studied by itself. 

Anaerobic germs may be cultivated in an atmosphere of hydrogen, 
the air in the closed culture receptacles being replaced by this gas. 
Or the oxygen may be removed from this confined portion of air in 
contact with the cultures by chemical means. A description of the 
various simple and complex devices for anaerobic cultivations falls 
beyond the scope of this work. 

The most scrupulous care is required in sterilizing the nutrient 
media and the utensils and instruments used, and the greatest caution 
should be exercised, in transferring the bacteria from one receptacle 
to another, to prevent contamination. A large experience in this 




Fig. 62.— Sterilized Cotton Swab in a Sterilized Tube for Collecting Fluids containing 

Bacteria. 

sort of manipulation is necessary before reliable results can be ob- 
tained in original investigation, since the slightest error or careless- 
ness in manipulation, or failure to observe the occurrence of contami- 
nation, are liable to entirely vitiate the results of long series of 
experiments. It is only by an extended preliminary training in the 
cultivation of some of the more characteristic and easily recognizable 
forms, under a variety of conditions, in a perfectly pure state, 
through a series of generations, that one can be assured of his 
capacity to carry on researches in this most difficult and intricate 
field. 

The methods of inoculation of animals with pure cultures, and the 
precautions to be observed, as well as a description of the various 
forms of apparatus made use of in practical bacteriology, must be 
sought in more extended treatises on this subject. 

It is wiser for one purposing to carry on bacterial researches to 
gain a practical acquaintance with methods and apparatus in a well- 
appointed laboratory, than to make the attempt to work out the 
methods from books. 

Material obtained from the human body which is to be subjected 



VEGETABLE PARASITES. 167 

to bacterial examination should be collected with every precaution 
against accidental contamination. 

A convenient mode of collection and transportation of small quan- 
tities of fluid or semi-fluid material, such as exudates, discharges, etc., 
for purposes of bacterial examination is to twist a small wad of ab- 
sorbent cotton on to the end of an iron or steel w 7 ire about five inches 
long, put this, swab end foremost, into the tube (Fig. 62), plug the 
mouth with cotton, and sterilize the whole in a dry oven for an hour at 
160° C. 

Several of these cotton swabs may be prepared at once and kept 
on hand. The swab, carefully removed and saturated with the 
material to be examined, is at once returned to the tube; this is 
plugged, and may be so safely transported. 

BACTERIAL EXAMINATION OP POST-MORTEM SPECIMENS. 

It is often important to make a thorough post-mortem examina- 
tion by cultures as well as morphologically of the blood and of all the 
viscera. This is not only important in those cases which during life 
gave clinical evidence of general infection, but also in many forms of 
disease whose nature is still wholly obscure. 

In the interpretation of the results of all such examinations, how- 
ever, it should be borne in mind that after death a new distribution 
of germs may occur, and that from the gastro-intestinal canal and 
from other surfaces or cavities of the body micro-organisms may, as 
decomposition progresses, penetrate the tissues and the viscera. 1 

A careful consideration of the general conditions under which the 
body has been kept and its state of decomposition is of especial impor- 
tance in the interpretation of the significance of the Bacillus coli 
communis, which is always present in such enormous numbers in the 
intestinal canal and which is not only apt to effect wide distribution 
in the body after death, but as a result of careless manipulation is 
liable to be accidentally brought in contact with other viscera after 
the opening of the gut. The preparation of cover slips for staining 
and the making of cultures is as a rule best done at the autopsy table- 
It is well as each organ is exposed — commencing with the heart — ■ 
to sear the surface of the organ to be examined with a broad-bladed 
knife heated over a flame, and then, making an incision through the 
seared surface with a sterilized scalpel, to press one of the above- 
mentioned sterilized cotton swabs into the opening and absorb the 
juices w T hich exude, or to pick out a small fragment of the solid 
tissue from the depths of the opening ; and then with the material thus 
procured make the required cultures and afterward the cover-slip 
smears for staining. 

1 Consult Achard and Phulpin, Arch, de rned. Experimentale, January, 1895. 



168 VEGETABLE PARASITES. 

If it be necessary to transport the material to the laboratory before 
making cultures, it is well to reserve the unopened organs, or large 
portions of these in the case of the solid viscera, and to wrap each 
separately in a cloth saturated with sublimate solution, or to put each 
in a separate sterile receptacle for transportation. 

Welch, Wright and Stokes, and Flexner have published the results 
of series of systematic post-mortem examinations of the viscera for 
bacteria. 1 

II. YEASTS. 

These micro-organisms — mostly saprophytes — consist of oval or 
spheroidal cells with granular protoplasm and a thin membrane. 
They multiply by sprouts or buds from the parent cell. The new in- 
dividuals may separate from the old, or may cling to them so that 
chain -like combinations may occur (Fig. 63). Some species of yeast 
set up fermentation in fluids containing sugar. Some grow to 




Fig. 68.— Yeast— Saccharomyces. 

a certain extent in the stomach and in the bladder in diabetes, but 
they appear to be usually of little importance in human pathology. 2 

III. MOULDS. 

The moulds are considerably more complex in structure than 
either the bacteria or the yeasts. Some of the forms are very common 
and universally known. In general, it may be said that the moulds 
consist of a series of delicate, translucent, jointed threads — my- 
celium — from which, either directly or through the intervention 
of a special structure, the sporangium, the spores are developed 
(Fig. 64). The moulds which are apt to occur in the human body 
may be of the former, more simple, or of the latter, more complex 
type. 

Among the simpler forms of moulds which occur in the body may 
be mentioned the Achorion Schonleinii, Microsporon furfur, Tricho- 
phyton tonsurans. There is a close morphological resemblance be- 
tween these forms. 



1 Welch, "A System of Surgery by American Authors, " Dennis, p. 311. Wright 
and Stokes, Boston Medical and Surgical Journal, March 21st and 28th, and April 
4th, 1895. Flexner, Trans. Assoc. American Physicians, 1896. 

- Rabinowitsch, "Pathogene Hefearten, " Zeitschrift f. Hygiene, etc., Bd. xxi., 
1S95. 



VEGETABLE PARASITES. 



169 



Achorion Schonleinii, the favus fungus, is formed of a much- 
branching mycelium from which the spores are directly developed 
{Fig. 65). It grows readily on artificial culture media, such as 
nutrient agar and gelatin, at the temperature of the body. This 




Fig. 64.— Aspergillus Glaucus. 
Showing mycelium, from which arise the spore-bearing structures. 

fungus is most apt to grow upon the hairy part of the head, where it 
forms small surface crusts and grows into the shafts and root sheaths 
•of the hair, exciting inflammation in the adjacent tissue. 




Fig. 65.— Achorion Sch5nleinii— Favus. 
From a culture. 



Trichophyton tonsurans develops in the form of a moderately 
'branching mycelium, forming comparatively few spores. It grows 
in the skin, either about or apart from the hairs, or in the nails, pro- 



170 VEGETABLE PARASITES. 

during the lesions of various phases of herpes, which differ consider- 
ably, depending upon the particular structures involved. At body 
temperature it grows readily on artificial culture media, differing 
markedly in appearance from Achorion, to which it is morphologi- 
cally quite similar. 

Microsporon furfur, the mould fungus causing pityriasis ver- 
sicolor, is more prone than the Achorion to the development of many 
spores, but otherwise considerably resembles it morphologically. It 
has not yet been cultivated on artificial media. By its infiltration of 
the epidermis, especially of the body and upper extremities, it causes 
larger and smaller yellowish or brownish patches. 

The more complex types of moulds are only occasional dwellers in 
the human body and appear to be but rarely the cause of disease, 
passing, rather, a saprophytic existence on dead material in parts of 
the body which are in communication with the air. Thus they may 
be found growing on accumulations in the external auditory canal, 
in dead tissue in the lungs, on walls of cavities, dilated bronchi, etc. 

A lowly form of micro-organism frequently found growing in the 
mouth and fauces and oesophagus of children, in the form of a whit- 
ish pellicle — aphthae — is the so-called Oidium albicans, which con- 
sists of branching, jointed threads and spores which penetrate be- 
tween the epithelial cells. This fungus may assume considerable 
importance, when in very feeble children it blocks the oesophagus, or 
when, as is rarely the case, from the surface of ulcers it penetrates 
the blood vessels and gives rise to visceral metastasis. The exact 
relationship of this fungus to the moulds is not yet very clear. 



METHODS OF STUDYING YEASTS AND MOULDS. 

The yeast organisms are in general stained and cultivated by the 
same methods as those used in studying the bacteria. The moulds 
may be simply teased and studied in glycerin or in glycerin and 
water. They may be stained with dilute aqueous fuchsin solution or 
with alkalin-methyl-blue solution (Loffler's solution, see page 158). 
When spores have formed in considerable numbers on the more com- 
plex forms of moulds, these are not easily wetted by the usual stain- 
ing fluids, because the air clings so closely among the spore masses. 
In a mixture of four parts of alcohol and one of aqueous solution of 
ammonia they are instantly wetted, and may then, with or without 
staining, be teased and mounted in glycerin. In studying the fun- 
gus masses in the above-described skin diseases it is well, when 
crust-like masses are to be teased apart, to allow them first to soak 
for a few moments in a flve-per-cent solution of caustic potash. In 
this solution they may be studied, or they may be teased and mounted 



VEGETABLE PARASITES. 171 

in glycerin for preservation. Most of the more common moulds are 
readily grown on the ordinary culture media. 1 

THE RELATIONS OF BACTERIA TO DISEASE. 

Bacteria are invariably present in greater or less numbers in the 
mouth, nose, upper air passages, gastro-intestinal and genito-urinary 
tracts of men and animals. 2 

Into these places they are more or less constantly brought by the 
respired air, by food and drink, and in other ways. But common 
and often a,bundant as are these germs upon the external and internal 
surfaces of the body, they do not pass through the healthy mucous or 
cutaneous surfaces, so that under normal conditions the tissues, the 
viscera, and the circulating fluids are germ-free. 

Except for certain pathogenic forms which may under unsanitary 
conditions have been set free and transported from men or animals 
suffering from infectious disease, the bacteria upon the cutaneous or 
mucous surfaces of the body are for the most part harmless ; while 
certain intestinal forms may even be useful in promoting digestion. 

Certain bacteria which do not often and some which never induce 
disease, find in or upon the human body such favorable conditions for 
their existence that they are commonly present there. The Bacillus 
lactis aerogenes and the Bacillus coli commune in the intestines, the 
Leptothrix in the mouth, the pyogenic and other bacteria of the skin, 
vagina, etc., exemplify the germs which find in the human body a 
favorite habitat. 

The body is guarded in various ways from the incursions of 
pathogenic and other bacteria, which may be commonly present or 
only occasionally lodged upon its surfaces. Among the protective 
agencies of the body may be mentioned the firm, dense skin which 
while intact protects the interior from the entrance of almost all 
known micro-organisms; the epithelial investment of the mucous 
membranes in several places swept by cilia; the protected situation 
of most of the mucous surfaces. 

Furthermore, the lymph nodes are important features in the pro- 
tective mechanism of the body, frequently filtering out of the lymph 
micro-organisms which have entered the body juices and holding 
them back from the general circulation. 

1 For resume and bibliography of relationship of yeasts and moulds to human 
diseases consult Bicker, "Ergebnisse der allg. Aetiologie des Menschen- u. Thier- 
krankheiten, " Abth. i., 1896, p. 892. 

2 For a summary, of facts concerning the bacterial flora of the body surfaces, con- 
sult Welch, " Surgical Bacteriology, " " System of Surgery by American Authors, " 
Dennis, p. 250 et seq. 



172 



VEGETABLE PARASITES. 



Finally, the power of certain of the body fluids and of living cells 
under favorable conditions to kill and dispose of germs, should these 
gain entrance through injuries or other structural lesions or func- 
tional disturbance in the barriers, is of great importance and will 
he referred to again. 

On the other hand, the cells and tissues in the vicinity of bacteria 
which have gained access to the body may show very marked alter- 
ations, which are presumably due to their influence. The cells may 
T)e swollen, their nuclei may break down or disappear, and the proto- 
plasm may be converted into a mass of shining or coarsely granulai 
particles, or may completely disintegrate. The intercellular sub- 
stance near the bacteria may also soften and disintegrate. In s 




Tig. 



-Bacterial Embolics in the Blood Vessels of the Glomerulus of the Kidney in 
Malignant Ulcerative Endocarditis. 



word, the tissue in their immediate vicinity is often found in a con 
dition of necrosis of one kind or another. The walls of blood vessels 
near which they lie may die, and the blood which these carry maj 
form thrombi. The bacteria may themselves enter the vessels anc 
proliferate in the blood ; they may be swept away as emboli to remote 
parts of the body (Fig. 66), and establish new foci of bacterial pro 
liferation and tissue necrosis. 

But the presence of the micro-organisms themselves is not neces- 
sary for the causation of small foci of necrosis in the tissues. Thes< 
may be caused by the toxic agents alone circulating in the bodj 
fluids (Fig. 6?). This form of lesion is very frequent in the infectious 



VEGETABLE PARASITES. 17$ 

diseases of the toxaemic type. Similar local effects may be induced 
by other poisons than those of microbic origin. 1 

Some bacteria, instead of inducing a simple necrosis, incite at the 
same time more or less intense inflammation (Figs. 68 and 294). This 
inflammation may be of a simple productive form, similar in its effects 
to that produced by the presence of any irritating foreign body ; or it 
may be active, progressive, and exudative in character ; or the bac- 
teria may determine, in some way as yet unknown to us, very pecul- 
iar and characteristic inflammatory changes, which result in the for- 
mation of new tissues of various kinds (see Tuberculosis). Some 
forms of bacteria find in the blood, others in the lymph spaces and 
vessels, the conditions most favorable for their proliferation. 

When we inquire more closely into the exact way in which these 






>■'-:.'/„> f • ♦ .-"V 



l# -" ... ® a 



> /" 



■■<& 



^ 



Fig. 67.— Small Focus of Necrosis ra the Liver caused by Toxic Material of Bacterial 

Origix. 

various deleterious effects are produced in the bod}' by pathogenic 
bacteria, we find that they are in but small measure simply mechani- 
cal. They appear to be largely due to the various chemical products 
eliminated or stored up in their protoplasm by the metabolism of the 
germs. These deleterious bacterial products may, as we have already 
seen, be those alkaloidal substances called poisonous ptomains or 
toxins, or they may be albuminoid substances — toxalbumins or tox- 
albumoses. Stored up in the protoplasm of the germs themselves, 
this poisonous material has been called b act erio -protein. 

The chemical constitution of these varied products is so complex 
and little understood, and the conditions under which they are 

1 Consult Flexner, "The Pathologic Changes caused by Certain So-Called Toxal- 
bumins, " ^Medical News, August 4th, 1894. 



174 



VEGETABLE PARASITES. 



developed, and the parts of the body to which they are spread and oi 
which they may act, are so varied, that it is not possible to mak 
very positive statements to-day as to their individual characters o 
the nature of their action. 1 Some of the poisons act locally at o 
near the seat of their manufacture by the growing germs. Other 
gain access to the body at large and are widely distributed, inducing 
what may be called the phenomena of septic intoxication — toxcemia 
The phenomena of septic intoxication may be induced by the pro 




"Fig. 68.— Colonies of Micrococci in a Blood Vessel op the Kidney, causing a Small Abscess 

From a case of pyaemia. 
Around the dilated and partially necrotic blood vessel in which the bacteria lie is an area c 
necrotic tissue and a small-celled infiltration or zone of pus. 

ducts of bacterial growth outside of the body when these in consider 
able quantity are in any way taken into it. This is true not only o 
poisons elaborated outside the body by pathogenic bacteria, but als< 
of many forms of bacteria usually harmless. Thus are caused mam 
forms of food poisoning which simulate but are not actually infec 
tious diseases, because there is no development within the body o 

1 Much of the literature on this subject has been brought together by Vaugha: 
and JSovy, "Ptomaines and Leucomaines, " 3d ed., 1896. The general chemica 
relationship of bacterial products to other organic compounds is set forth in Halli 
burton's "Text-Book of Chemical Physiology and Pathology. " 



VEGETABLE PARASITES. 175 

the disease-producing germs. It should be remembered also that toxic 
effects closely resembling those due to bacterial poisons may be caused 
by toxic agents developed within the body as a result of defective 
elimination or faulty cell metabolism. 

It has been found that the proteid constituents of the protoplasm 
of various species of bacteria, both parasites and saprophytes, are 
capable, when set free by the disintegration of the germs in the body, 
of attracting leucocytes in large numbers to their vicinity. This 
drawing of living cells by chemical agents is called chemotaxis, 1 and 
it seems probable that the gathering of cells in suppurative foci may 
be due to the chemotactic power of the bacterial protein of the disin- 
tegrating germs which have gathered there. 2 This chemotactic 
power is not confined, however, to the bacterial protein, but is ex- 
hibited by proteids from a great variety of sources. It has further- 
more been shown that bacterial proteids are capable of stimulating 
cell proliferation. This has been shown in the case of leucocytes and 
many other forms of cells (see action of the bacterial protein of the 
tubercle bacillus, page 223). 

It will be seen, from what has now been said of the bacteria, that 
in different parts of the system in health, and in a large number of 
abnormal conditions, various forms of bacteria occur; but it is quite 
evident that the significance which we must attach to their mere 
presence varies greatly. In a large number of cases, especially when 
on parts exposed to the air or in the gastro-intestinal canal, they are 
evidently of no more importance than so much inorganic dust. 
When, however, special forms of bacteria are found to occur uni- 
formly in connection with well-defined diseases, or in their lesions, 
the conjecture is certainly justified that they may have something to 
do with their production. Yet in all such cases we have to consider 
the possibility that it is the abnormal state of the body or the char- 
acter of the lesion, produced perhaps by other causes, which affords 
conditions suitable for bacterial growth, and that they may conse- 
quently occur in considerable numbers, while in the absence of these 
conditions they would be unable to develop. Even the constant 
occurrence in the body, in certain diseases, of bacteria which evi- 
dently produce well-marked local effects, either inflammatory or 
degenerative, does not absolutely prove their causative relation to the 
disease, although it renders it in a high degree probable. 

It is desirable in every case in which the evidence of the causa- 
tive relationship of a specific micro-organism to a disease is to be set 



1 Negative chemotaxis is the repelling of living cells by chemical substances. 

2 For a resume of observations on chemotaxis see New York Medical Journal, 
June 6th, 1891. 



176 VEGETABLE PARASITES. 

forth, that we should be able to demonstrate the constant presence in 
the body of the special form of micro-organism, obtain this by cul- 
ture in a pure condition unmixed with any other living thing or with 
any chemical substance not belonging to it, and finally, by the intro- 
duction of the purified organisms into a healthy animal, be able to 
produce the disease in some definite form. When all this is done, 
and not before, can we assert that the evidence establishing the cau- 
sative relationship between a given form of bacteria and any special 
infectious disease, is entirely at our command. 

But the fulfilment of these strict logical requirements is very diffi- 
cult in many cases, and in some, apparently, almost if not quite 
impossible; for we must remember, in the first place, that the lower 
animals, upon which alone, for the most part, inoculation experi- 
ments are practicable, are apparently not subject to certain important 
diseases of man; and, second, that they present among themselves the 
most marked differences in the degree and manner in which they 
are affected by inoculation with pathogenic bacteria. Desirable as is 
the complete fulfilment of the above requirements in ever} 7 case, it 
must be admitted that a reasonable certainty regarding the bacterial 
origin of a given disease may be arrived at without positive results 
from the inoculation of the bacteria associated with its lesions. 

The discussion of the probabilities of the bacterial origin of cer- 
tain classes of disease, and the long series of phenomena exhibited by 
them, which the bacterial theory very satisfactorily explains, does 
not fall within the scope of this book. 

The complete demonstration which is desirable has as yet been 
furnished in but a moderate number of cases. In many others, how- 
ever, enough has been done in the way of study and experimentation 
to render it altogether certain that the diseases are infectious and to 
establish beyond reasonable doubt the identity of the micro-organism 
or micro-organisms involved. 

Conditions Influencing the Occurrence of Infectious Diseases. 
— It has been learned, as the result of a great deal of observation 
and experiment, that although certain diseases are invariably caused 
by the presence and growth in the body of particular species of 
micro-organisms, and never occur without them, there are still vari- 
ous other accessory factors which have an important bearing upon 
the inception and course of the diseases. Thus, while the pres- 
ence in the body of a particular species of micro-organism is the- 
most significant and fundamental of the determining agencies in the 
infectious diseases, the numbers in which they are present — i.e., the 
size of the dose — and the varying virulence which the same species 
under different conditions possesses, as well as the varying capacity 
of resistance to the incursions of the germs which the body cells at 



VEGETABLE PARASITES. 177 

different times and under differing conditions exhibit, are all factors 
of the greatest moment. 

It should be always borne in mind that the human body is a great 
aggregate of groups of co-ordinated cells which, under normal con- 
ditions, all act in harmony for the maintenance of the life and func- 
tions of the individual. The cells and cell communities in health not 
only do this, but they have the power of resisting and to a certain 
extent overcoming the various deleterious agencies to which the body 
is more or less constantly liable. 

What we call hereditary or acquired predisposition to an infec- 
tious disease, such as tuberculosis, for example, is simply a lack of 
the usual capacity of the cells of the body — whether through a struc- 
tural or physiological fault we do not yet know — to cope with the 
destructive tendencies of the living micro-organisms when once these 
gain a foothold in the body. 

We thus see that, in studying the conditions under which infec- 
tious diseases occur, the work is by no means complete when we have 
demonstrated the bacterial species which causes the disease, but that 
then the more obscure determining and influencing agencies must be 
worked out in each particular case. 

INFECTION AND IMMUNITY. 

An infectious disease is one caused by the entrance into the 
body and proliferation there of pathogenic micro-organisms. 

The fact that all animals are not equally susceptible to the ravages 
of pathogenic micro-organisms, and that in man an individual and 
often a changing predisposition or invulnerability to the incursions 
of these organisms exists ; the further observation that one attack of 
an infectious disease often protects the victim for a longer or shorter 
time against a recurrence; finally, the fact that recovery is ever 
possible when once self -multi plying disease-producing germs have 
obtained a foothold in the body — all these facts and observations 
are of such singular import and interest that, especially of late years, 
much study has been expended on the nature of the forces which the 
body brings into play in establishing immunity in the face of micro- 
bic invasion, and in coping with the various deleterious agencies at 
work when once a foothold is obtained. The scope of this book does 
not permit us to enter in detail into this most fascinating and im- 
portant field. But some conception of recently acquired facts is in- 
dispensable for the comprehension of acute infectious diseases and 
of the lines along which we may confidently anticipate success by 
new methods of treatment. 

Immunity is insusceptibility, or capacity for resistance on 
the part of the body, to infection or its effects. 
15 



178 VEGETABLE PARASITES. 

Immunity from an infectious disease may be hereditary. 

Thus our domestic animals eujoy a natural or hereditary im- 
munity from many of the infectious diseases of man; while amonc 
themselves some animal species are susceptible, others not, to the same 
disease. 

On the other hand, immunity may be acquired. Acquirec 
immunity may be effected by an attack of the disease from whicr 
the individual has recovered — natural immunization — or by th( 
introduction into the body of some material which gradually dimin 
ishes susceptibility without inducing distinct disease — artificial im- 
munization.. Acquired immunity may be transmitted from paren 
to offspring. 

Most of the infectious diseases appear to confer a certain degree 
of insusceptibility to subsequent attacks of the same disease, thougl 
this may be partial and temporary. But the exanthemata afford the 
most striking examples of acquired immunity after an attack of in 
fectious disease. 

It is well known that bacteria artificially introduced into the 
blood of animals may after a short time wholly disappear from the 
circulating fluid and be found in large numbers in leucocytes anc 
other cells. 

It is believed that certain cells of the body are capable not only oj 
taking up micro-organisms which get into the tissues, into their pro 
toplasm, but of there killing and perhaps digesting them, and tha" 
thus the destruction of germs in the body may be brought about. 
The cells which take up into their bodies the micro-organisms, sa 
well as other foreign bodies, are called phagocytes. This mode oj 
destruction of micro-organisms, largely by leucocytes but also bj 
other mesodermal cells, forms a most suggestive and fascinating 
study, but its full significance and importance are not yet deter 
mined. 

On the other hand, certain albuminous ingredients of the bod} 
juices, "alexins" or "defensive proteids," have been shown to pos 
sess marked germicidal powers, which may be of extreme importance 
in protecting the organism. But how important this is we cannoi 
yet say. 

While thus two fairly distinct influences are believed to be oj 

1 The elimination of micro-organisms from the body through its secretions, sucl 
as urine, bile, milk, sweat, saliva, etc., is a matter of great significance, but whicl 
the scope of this book does not permit us to enter upon. Consult Sherrington, "Ex 
periments on the Escape of Bacteria with the Secretions," Journal of Pathology 
and Bacteriology, February, 1893 ; Biecll and Kraus, Arch. f. exp. Path., Bd. 37, p. 1 
1895, Bibliography; and Hintze and Lnbarsch. "Ergebnisse der allg. Aetiologie de: 
Menschen- und Thierkrankheiten, " 1896, p. 287. 



VEGETABLE PARASITES. 179 

importance in enabling the body to resist the incursions of patho- 
genic germs — cellular or " phagocytic" and what may be called the 
" humoral" or chemical — it is obvious that ultimately whatever pro- 
tecting power the body possesses must be due, directly or indirectly, 
to cell activities. 3 

But however incomplete our comprehension, may be of the exact 
nature of the protective agencies of the body against pathogenic 
micro-organisms, the clinical and experimental data have led to and 
steadily encouraged the hope that artificial immunization might 
become an important factor, both in the prevention and in the 
treatment of certain forms at least of infectious disease. 

If we briefly summarize the results of a vast amount of the most 
painstaking research in this direction, we find that in fact artificial 
immunization can be accomplished in several ways. These processes 
of artificial immunization depend upon gradually rendering the 
body tolerant in one way or another to the presence of the infec- 
tive agencies without actually inciting the characteristic specific 
disease. 

I. In one class of procedures artificial immunity is conferred 
directly or indirectly through the action in the body of bacteria 
or bacterial poison tvhose virulence has been in one way or 
another reduced but not rendered altogether inert; or by the action 
in the bodies of relatively insusceptible animals of germs or germ 
poisons of unimpaired virulence. 

1. Insusceptibility to particular forms of infectious disease may 
be conferred by inoculation with cultures whose virulence has been 
artificially reduced. This reduction of virulence of the micro- 
organisms may be accomplished in various ways — by cultivation at 
temperatures above their optimum ; by successive inoculations into 
insusceptible animals; by prolonged artificial cultivation in the pres- 
ence of oxygen ; by exposure to certain inorganic chemical substances, 
as the diphtheria bacillus to trichlorid of iodin, anthrax to bichromate 
of potash, etc. ; by exposure of cultures to organic extracts or products 
of animal or vegetable cell metabolism ; by drying or by exposure to 
sunlight; and in other ways. 

With the virulence of the micro-organisms reduced in varying 
degrees in one or other of the ways just mentioned, the gradual hab- 
ituation of the bodies of animals to the presence of pathogenic germs 
may be pursued until cultures of full virulence are tolerated. 



1 For a summary of the prevalent views on the cellular theory of immunity, with 
bibliography, consult Metschnikoff. "Ergebnisse der allg. Aetiologie der Menschen- 
und Thierkrankheiten, " 1896, p. 298. For a summary of the chemical aspects see 
Frank, ibid., p. 344. 



180 VEGETABLE PARASITES. 

2. Immunity may be conferred by the injection, in gradually 
increasing doses, of the metabolic products of bacterial growth, 
either with or without the dead bodies of the germs themselves. The 
primary virulence of these usually toxic products of microbic growth 
may be in various ways diminished, by heating, by mixing with 
organic extracts such as that of the thymus gland, or with an inor- 
ganic chemical substance such as trichlorid of iodin. 

3. Immunity may be secured in some cases by the inoculation of 
animals which are but moderately susceptible to the species employed, 
with small but increasing quantities of germs having unimpaired 
virulence. Under these conditions the animal becomes more and 
more unresponsive to the germ, until finally be may display no reaction 
after a quantity of the virulent culture which at first would have 
been inevitably fatal. Thus gray mice have been gradually made 
refractory to the typhoid bacillus, many animals to the diphtheria 
bacillus, etc. 

II. In a second class of procedures artificial immunity is 
conferred by the direct mingling of the body fluids of an al- 
ready immune individual with those of the individual to be 
protected. 

1. Extracts of various organs and tissues of animals suffering 
from infectious disease, rendered germ-free and injected into healthy 
animals, have been found in some cases to confer a certain degree of 
immunity. 

2. The blood serum of animals naturally immune to a particular 
infectious disease has been found on injection into those which are 
susceptible to the same disease to impart in some cases a certain 
degree of insusceptibility. 

3. The blood serum finally of animals which have been rendered 
in oneway or another artificially immune to certain diseases, if intro- 
duced under proper conditions into another susceptible animal, has 
been found not only to confer a temporary immunity, but if admin- 
istered to an already stricken individual to aid him in the most 
marked and efficient way to overcome the deleterious agencies at 
work. 

The knowledge of this immunizing and curative action of specially 
endowed blood serum has been most fully developed in diphtheria and 
tetanus. The application of a wide range of facts experimentally 
revealed in the lower animals has led to the opening of a new method 
for the prevention and control of infectious disease, which under the 
name of serum- therapy is not only full of promise but has already 
proved to be of inestimable practical value. 

The fact that many of the pathogenic micro-organisms act harm- 
fully upon the body largely through their self -engendered toxins, and 



VEGETABLE PARASITES. 181 

that the effect of the introduction of the blood serum of artificially 
immunized animals appears to be to neutralize this deleterious effect, 
has led to the use of the word antitoxin for the substance or sub- 
stances, still unknown, which the serum of the immunized animal is 
presumed to contain. 

The facts which have just been set forth seem to indicate that 
in the artificial immunization we are bringing into play and rein- 
forcing the conservative agencies which under natural conditions 
the body commands. In the direct immunization of animals by the 
toxic product of germ metabolism considerable time is consumed 
in rendering available the protective agencies which the body finally 
secures. 

On the other hand, in the employment of the blood serum of arti- 
ficially immunized animals for protective and curative purposes we 
make use of the accomplished results of the protective mechanism of 
one animal for the more direct, speedy, and certain protection of 
another, and this effect is produced without those evidences of pro- 
found disturbance which the use of toxic agents frequently discloses. 
Moreover, the efficiency of the immunizing or curative blood serum 
is directly proportionate, as a rule, to the degree of immunity which 
the animal from which it is derived enjoys, and upon the amount of 
serum, or, which is the same thing, the amount of antitoxin intro- 
duced. Whether this substance, antitoxin, acts by directly neutral- 
izing the poison which is determining the manifestations of the 
infectious disease, or whether, as seems on some accounts more prob- 
able, it stimulates the body cells which constitute the natural pro- 
tective mechanism of the stricken individual to greater activity or 
to more purposeful accomplishment — these are questions of great 
theoretic interest which the knowledge of to-day does not enable us 
definitely to answer. 

In the case of diphtheria the perfection of the process of artificial 
immunization and the establishment of a definite and successful 
curative method are the direct results of a long, patient, logical series 
of animal experiments with a definite end in view and by the use of the 
absolutely identified and well-known germ which causes the disease. 
On the other hand, it is not a little curious that in small-pox and in 
hydrophobia effective methods of immunization should have been 
perfected absolutely without knowledge of the micro-organisms which 
cause the diseases, and yet by procedures which, though somewhat 
empirically hit upon, are nevertheless in close accord with those 
which the most recent studies on immunitj- in general have shown to 
be effective. Thus in both small-pox and hydrophobia the material 
used for protective inoculation is that which has been artificially 
reduced in virulence; in the one case — small-pox — by its passage 



182 VEGETABLE PARASITES. 

through the body of a relatively insusceptible animal ; in the other — 
hydrophobia — by drying in the air (see pages 272 and 277). l 

1 For a fuller treatment of the themes considered in this section the reader may 
consult the admirable article by Welch, "General Considerations Concerning the Biol 
ogy of Bacteria, Infection and Immunity, " " Text-Book of the Theory and Practice of 
Medicine, "Pepper. Hueppe's "Naturwissenschaftliche Einfiihrung in die Bakterio- 
logie " is an excellent rational summary. For fuller exposition and bibliography see 
Sternberg' 1 s "Immunity, Protective Inoculations, etc. " 

The most comprehensive treatise on bacteriology is Sternberg's "Manual of Bac- 
eriology. " The works of Heim, Rueppe, Frankel, Qiinther, Baumgarten, Klemperer 
and Levy, and of McFarland, contain valuable technical and historical data. 

The best laboratory manual for beginners is Abbot's " Principles of Bacteri- 
ology, " 3d ed., 1895. 

A comprehensive annual review of bacteriology, especially in its relations to the 
infectious diseases of men and animals, and indispensable for reference, is Baum- 
garten' s " Jahresbericht iiber die Fortschritte in der Lehre von den pathogenen 
Mikroorganismen. " 

Lubarsch and Ostertag's "Ergebnisse der allg. Aetiologie der Menschen- u 
Thierkrankheiten " contains valuable resumes and bibliography. 

A large part of the record of recent detailed study is widely scattered in mono- 
graphs and journals. 



THE INFECTIOUS DISEASES. 



Infectious diseases are those which are caused by the entrance 
into the body aDd proliferation there of pathogenic micro-organisms. 
Infection is the act or process by which such diseases are caused. 
In the more exact usage of the words infectious and infection which 
our new knowledge demands, it is customary and convenient to limit 
the term micro-organism to the fungi — bacteria, yeasts, and moulds 
— and (representing the animal kingdom to the protozoa), excluding 
altogether the entozoa and other animal parasites. 1 

The modern conception of infection implies' the presence in the 
body of the living micro-organisms themselves, that is of something 
capable of multiplication, and not alone of the poisons which they 
may and usually do produce. It is customary to look upon the effects 
of the absorbed poisons which micro-organisms produce as intoxica- 
tions^ whether these poisons be formed inside the body in infectious 
diseases or outside of it and subsequently introduced. That condition 
in which there is evidence of wide distribution of pathogenic micro- 
organisms and their products in the blood is called septicemia. On 
the other hand, toxaemia may be appropriately used to indicate the 
condition in which, with a situation and development of micro- 
organisms largely local (or outside of the body altogether), such 
constitutional disturbance exists as indicates the distribution of toxic 
products in solution. 

From this point of view diphtheria and tetanus are infectious 
diseases of the toxemic type, while general anthrax infection and some 
of the severer phases of infection with pyogenic streptococci repre- 
sent the septicsemic type. But it should not be forgotten that the 
greatest diversity exists in the local and general manifestations of 
infectious diseases, not only among the different diseases but also in 
the same disease ; in different individuals, and even in the same 
individual at different times. 



1 With this somewhat arbitrary limitation, neither trichinosis nor scabies, for ex- 
ample, would be considered an infectious disease. 

2 Intoxication phenomena, in this sense, are not limited to those caused by the 
metabolic products -of the fungi, whether parasites or saprophytes, but may be 
induced by various animal products also — snake venom for example. 



184 THE INFECTIOUS DISEASES. 

With this diversity in view, one may for convenience assort the 
cases of infectious disease into : 1st, Those in which the manifesta- 
tion of the disease is limited to a local lesion : 2d. Those in which 
there is, with or without demonstrable evidence of the seat of thifc 
local lesion, either (a) such constitutional disturbance as indicates 
distribution of toxic products, without dissemination of the micro- 
organisms themselves ; or (b) a general dissemination of the micro- 
organisms as well as their toxic products. But if this grouping be 
adopted it should be with the clear understanding that such distinc- 
tions are applicable only in the comparatively few wholly typical 
manifestations of infection. For in most cases transitional phases, 
varying susceptibility, and doubt as to the place and nature of the 
primary lesion render difficult or hopeless the maintenance of close 
distinctions. 

To-day we know definitely the particular organisms which cause 
some of the infectious diseases, and this knowledge, absolute and pre- 
cise as it is in particular cases, enables us to assume with greatei 
confidence than has hitherto been possible that the causative factor 
which in certain others of similar general characters still eludes us, 
will, when discovered, prove to be micro-organisms capable of indefi- 
nite multiplication and closely allied to those with which we are to- 
day familiar. 

Mixed or Concurrent Infection. — It should always be borne in 
mind that the body which is already the seat of an infectious disease 
is usually especially susceptible to the action of other pathogenic 
germs, should these once gain entrance; and also that the lesions 
which are associated with many of the infectious maladies afford 
portals of entry through the skin or mucous membranes to other 
micro-organisms, against the entrance of which the healthy body 
opposes most efficient barriers. In fact, we now know that the action 
of two or more pathogenic micro-organisms in the body at the same 
time is of very frequent occurrence, many of the so-called complica- 
tions of the infectious diseases being due to secondary infection with 
a new germ species. 

Numerous examples of this "mixed" or, better, "concurrent," in- 
fection are noticed in other parts of this book. 

A great many important facts have been revealed by the study of 
bacterial association in cultures as well as in infectious diseases of 
men and animals which cannot here be considered. 1 It may be said 
in general that in animals as in man the concurrent infection with a 
second micro-organism increases the gravity of the original situation. 

On the other hand, certain series of experiments seem to indicate 

1 Consult Th. Smith, Trans. Association American Physicians, vol. 9, p. 85, 
1895. 



THE INFECTIOUS DISEASES. 185 

that the concurrent action of other germs — streptococci, for example, 
with the anthrax bacillus— may render the latter comparatively 
innocuous. But the conditions of the experiments are in either case 
so complex that the full significance of many curious phenomena is 
not yet apparent. 

Congenital Infections. — Infection of the foetus through such 
lesions of the placenta as permit of the passage of pathogenic micro- 
organism from the blood of the mother to tha£ of the child is of 
occasional, but not frequent, occurrence. 

While the barriers against such transmissions are, under normal 
conditions, effective, disturbance in the placental circulation, lesions of 
the vessel walls or of the tissues and covering of the chorionic villi 
favor it. But infection may occur without demonstrable evidence 
of such lesions. 

Thus foetal infection is known to have occurred in various phases 
of suppurative inflammation, in tuberculosis, typhoid fever, anthrax, 
syphilis, the exanthematous fevers, etc. There is considerable evi- 
dence that rarely the tubercle bacillus may be transmitted from 
mother to offspring, and remaining for a time inactive may later 
induce the characteristic lesions. 1 

Terminal Infections. — The victims of chronic disease of the 
heart, blood vessels, kidneys, liver, etc., are particularly susceptible 
to the incursions of pathogenic micro-organisms and to infectious 
diseases of one kind or another. Such persons, with or without 
definite lesions, are in fact liable finally to succumb to the complicat- 
ing disease. 

The phrase " terminal infection" has been applied by Osier and 
others to this concurrence of diseases of such different nature, in 
which the chance infection of a vulnerable organism is so apt to 
prove fatal. 2 

Communicability of Infectious Diseases. — It is important in 
practical dealings with the infectious diseases to consider them in the 
light of the relative liability of transmission of the actually known or 
assumed micro-organisms from diseased to healthy individuals. 

In the first place, it should be borne in mind that the lower 
animals are insusceptible to the ravages of some of the micro- 
organisms which readily incite infectious disease in man. Thus 
the lower animals are, so far as we know, naturally immune to 
syphilis. To certain diseases of the lower animals, on the other hand, 
man is not subject. But to certain other infectious diseases, tubercu- 

1 For bibliography and summary of foetal infection see Lubarsch, "Ergebnisse 
der allg. Aetiologie der ATenschen- unci Thierkrankheiten, " 1896, p. 427. 

2 For a study of this class of cases see Flexner, Transactions Association American 
Physicians, vol. xi., 1896. 

16 



186 THE INFECTIOUS DISEASES. 

losis, for example, both men and the lower animals are liable and 
both are, in fact, under the prevailing conditions of modern life, fre- 
quent victims. 

So far as the liability to the transmission of the infectious agents 
from man to man is concerned, there is a very marked and signifi- 
cant difference between the infectious diseases. It is common usage 
to speak of the transmission or communication of disease, as if 
disease were a self -existent thing. This usage fosters much loose 
thinking. What we call disease is a departure from, failure in, or 
perversion of normal physiological action, either in the material con- 
stitution or in the functional integrity of the living organism. 
When, therefore, we speak of the transmission or communication of 
disease, what we really mean is not that the disease, but the agent 
capable under suitable conditions of inciting the disease, is trans- 
mitted or communicated. If we hold this obvious implication in 
mind, however, it is convenient to group the infectious diseases of 
man into two great primary classes: 1st, Those which under the 
usual conditions of life are not communicable. 2d, Those which 
under the usual conditions of life are communicable. 

There are then two classes of infectious disease : the non-com- 
municable and the communicable. In the first class are malaria 
and yellow fever. In the second class are all the rest. Among the 
communicable infectious diseases there exists, however, the widest 
difference in the liability to transmission under ordinary circum- 
stances. Thus the infectious agents in small-pox and scarlatina are 
given off from the body under such conditions as to render possible 
and frequent their direct transmission through the air to another 
individual. In syphilis, tetanus, and rabies, on the other hand, trans- 
mission of the infectious material is rare or impossible without a 
direct inoculation. 

Between these extremes the widest diversity exists in the liability 
to transmission of the infectious agents of the diseases of this class. 
In fact the liability to infection on the part of a healthy individual in 
the presence of a victim of infectious disease is largely dependent 
upon the intelligent care which is exercised in the disposition of the 
material containing the pathogenic micro-organism which in one way 
or another the infected body sets free. 

So that while it may be useful to arrange the communicable in- 
fectious diseases in groups or in such serial order as may indicate 
the degree of communicability of each under the ordinary conditions 
of life, it should always be borne in mind that this classification is 
not fundamental as is that by which the infectious diseases as a whole 
are set apart from other morbid states, but is closely dependent upon 
the sanitary conditions under which each case may be placed. Thus 



THE INFECTIOUS DISEASES. 187 

tuberculosis or diphtheria or pneumonia may be high on the list as 
readily communicable, if housed in a crowded tenement with igno- 
rant or careless attendance, while if subjected to the intelligent min- 
istry of sanitary science these diseases may be accounted as relatively 
slightly communicable. 1 

1 Before the knowledge of pathogenic micro-organisms had become precise, 
readily communicable diseases were called contagious in a rather loose and ill-defined 
way, and the unknown causative agent was called the contagium. The word con- 
tagious is still used, in various senses, to the detriment of science. We can get 
along well enough without it by the use of the word communicable in the way 
above indicated. But if it must still be cherished it might be most safely limited to 
the exanthemata, whose inciting agents are more readily and commonly transmitted 
through the air from the body of the patient than are those of any of the other 
infectious maladies. 



INFECTIOUS DISEASES INDUCED BY THE "PYOGENIC 

BACTERIA." 

There are many very important inflammatory lesions, close! 
allied in their character, and commonly, though not always, asso 
ciated with suppuration, which are due to the presence and growtl 
in the body of the spheroidal bacteria or cocci known as Staphylc 
coccus pyogenes and Streptococcus pyogenes. While other micrc 
organisms may and frequently do induce suppuration, these are com 
monly considered as par excellence the pyogenic bacteria. 1 

SUPPURATIVE INFLAMMATION. 

We will first consider the morphological and biological character 
of these germs and their relation to suppurative inflammation, am 
then, in order, the other special forms of disease with which the; 
are associated. 

The Staphylococcus pyogenes aureus (Fig. 69) is in general , 



Ml?/ 



&&&> 
*•:»$••*• 



Fig. 69.— Staphylococcus Pyogenes Aureus. 
From a beef -tea culture. Stained with geutiau violet. 

small coccus, the individuals varying, however, considerably in siz 
(0.7-1.2 <j- in diameter). In its growth it does not show a charac 
teristic grouping, but grows in irregular masses and heaps (th 
somewhat crude resemblance, when studied under a cover glass, to 
bunch of grapes gave rise to the generic name) ; sometimes, however 
pairs and groups of four or short rows of the cocci are seen. The gerr 
is readily stained by the anilin dyes, and does not lose its color i 

1 It should be borne in mind that while a limited suppurative inflammation ca 
be incited by chemical agents, such as ammonia, turpentine, etc., in the great rrn 
jority of cases it is incited and sustained by micro-organisms or their metabolic proc 
ucts. 



THE INFECTIOUS DISEASES. 189 

Gram's method of staining. It does not show spontaneous move- 
ment, and, like other spheroidal forms, does not appear to develop 
spores. It is quite tenacious of vitality, surviving long drying and 
degrees of heat and cold and an exposure to chemical bactericides to 
which many pathogenic germs readily succumb. It grows well at 
ordinary room temperature in such artificial culture media as nutrient 
gelatin, agar, beef tea, and milk, and on potatoes, forming some- 
what voluminous masses of culture. It rapidly fluidifies gelatin, 
coagulates milk, and in the various media develops a yellowish- 
white or a deep golden-yellow color, whence its specific name, 
aureus, and its common name, "golden coccus." Its color-produc- 
ing capacit}' is subject to wide variation. The virulence of cultures 
obtained from different sources varies a good deal, but in general sup- 
puration is not readily induced in the lower animals by its subcutane- 
ous injection. Liability to suppuration is greatly increased b} r 
mechanical or chemical injury to the tissues with which the germ is 
brought in contact. 

Injection of a virulent culture into the ear vein of the rabbit is 
usually followed by multiple abscesses in the kidney and muscles, 
and by suppuration of joints, etc. 

In man this coccus grows readily and rapidly, and may cause 
necrosis and exudative inflammation, especially its suppurative 
phases (Fig. 70). The lesions which it induces are apt to be cir- 
cumscribed. It may cause pustules, boils, and abscesses, and various 
suppurative inflammations of the viscera and serous membranes, 
joints, bones, endocardium, etc. These effects may be induced by 
the staphylococcus alone or by it in association with other species of 
germs. Its relationship to pyaemia will be considered under that 
heading. 

The Staphylococcus pyogenes aureus apparently produces its 
effects in the body in virtue of certain toxins or toxalbumins which 
are produced as the result of its metabolism, and which are either at 
once set free or stored up in the body of the germs until their release 
by disintegration after the death of the germs. The special power of 
the staphylococcus to cause the gathering of leucocytes is doubtless 
due to the marked chemotactic powers of some of the proteid sub- 
stances in its protoplasm. But here, as with other pathogenic germs, 
we shall do well not to be too precise in assigning closely the minute 
phases of lesions to definite chemical products of germ metabolism ; 
because these are very complex indeed, and our field of observation 
on them is but newly opened. Nor is our knowledge of the particular 
element in the germ or its products which is prone to induce necrosis 
at all precise. 

The Staphylococcus pyogenes may obtain entrance to the body 



190 THE INFECTIOUS DISEASES. 

through wounds, small or large, of the skin or mucous membranes. 
The possibility of its entrance through uninjured surfaces has been 
demonstrated. In many cases we are quite unable to trace its mode 
of access. While in the natural course of events this germ tends to 
die in the body, it may yet remain for a long time alive. 

It is widespread in inhabited regions, especially in towns, being 
frequently found on the surface of the body, and in the saliva, 
especially of those with acute or chronic catarrh of the upper air pas- 
sages. As the result of the filthy habit of indiscriminate public spit- 
ting, it is common in the dust of hospitals, houses, towns, and places 
of public assembly. 

Staphylococcus pyogenes albus. — This appears to be a variety of 







.• • • 



•v 



Fig. 70.— Staphylococcus Pyogenes Aureus, in and among the Pus Cells, from an Abscess 

of the Kidney. 

the Staphylococcus pyogenes aureus which does not develop the yel- 
low color in cultures. It is of frequent occurrence both in connection 
with the aureus and alone. Its action on the body is similar, but it 
has seemed to many observers to be in general less virulent. 

Staphylococcus epidermidis albus. — This coccus has been de- 
scribed by Welch ■ as of frequent occurrence in the epidermis, and 
although of rather feeble pyogenic power, yet seems frequently to 
cause small stitch abscess and moderate suppuration along drainage 
tubes. Welch regards it as possibly a variety of Staphylococcus 
pyogenes albus. 

1 Welch, "Wound Infection," American Journal of the Medical Sciences, voL 
cii., p. 457, 1891. 



THE INFECTIOUS DISEASES. 191 

The Streptococcus pyogenes is distinguished morphologically 
from the cocci just described by the marked tendency which the in- 
dividuals exhibit, when growing, to hang together in longer or 
shorter chains (Fig. 71). It is like the Staphylococcus pyogenes, 
immobile, and stains easily in the same way. 

It grows readily, but more slowly than Staphylococcus pyogenes, 
on the ordinary culture media. It does not fluidify gelatin, on which 
it grows as small, inconspicuous, grayish-white colonies. On the sur- 
face of agar plates kept in the thermostat at 37° C. for twenty-four 
hours, the small grayish colonies usually show, under the microscope, 
loops and fringes of the chain-like cocci extending off from the bor- 
ders. The growth on potatoes is inconspicuous. In nutrient broth 
it usually forms delicate, flocculent masses, which cling to the sides 
of the tubes, leaving the fluid clear. Occasionally the masses of 
streptococci are dense and compact. Not infrequently the growth 
is diffused through the nutrient broth, rendering it turbid. 

"When in vigorous growth it coagulates milk. 




Fig. 71.— Streptococcus Pyogenes. From a broth culture. 

There is considerable difference in the tenacity with which, in 
broth cultures of streptococci from different sources, the individual 
cocci cling together, so that in one set of cultures the chains may 
be very long, in another short. It has been thought by some observ- 
ers that this difference was so constant as to justify special names 
for these growth variants of the streptococcus, and they have been 
called respectively Streptococcus longus and Streptococcus brevis. 
The growth in dense masses has given rise to the name Streptococcus 
conglomeratus. It is questionable, however, whether these names 
should be considered as implying more than rather inconstant growth 
varieties. 

Streptococci which give evidence of little virulence in animal 
inoculation are very common in the mouths of healthy persons. The 
significance of these germs in healthy mouths is not yet clear. 

The results of animal inoculation with the Streptococcus pyogenes 
are in general -similar to those with the Staphylococcus pyogenes 
aureus, but its effects are rather less marked and its action more 



192 THE INFECTIOUS DISEASES. 

uncertain. The streptococcus is very frequently associated with 
Staphylococcus pyogenes aureus both in its distribution outside the 
body, in healthy persons, and in disease. In general it may be said 
that the streptococcus incites those forms of suppuration and flbro- 
purulent inflammation which tend to spread both locally and through 
metastasis. 

We may summarize the prominent local effects of the pyogenic 
cocci in the body by saying that they tend to induce the gathering of 
leucocytes by chemotaxis, they stimulate cell proliferation, and they 
are prone to induce tissue necrosis. 

Staphylococcus pyogenes and Streptococcus pyogenes have been 
found, either separate or in association, in a large number of sup- 
purative processes in various parts of the body, the condition in 
some cases receiving special names, in others not. Thus in boils and 
carbuncles, in abscesses and phlegmons, in herpes, impetigo and 
panaritium, in phlebitis and lymphangitis, in suppurative inflamma- 
tion of various mucous and serous membranes, and in some forms of 
pneumonia, one or other or both of these germs are frequently con- 
cerned. 2 

One of the most important features of the relationship of Strepto- 
coccus pyogenes to man is the frequency with which it enters as a 
concurrent pathogenic agent in already established infectious diseases 
due to other forms of micro-organisms. Thus some of the most 
serious complications to which the victims of scarlatina, diphtheria, 
typhoid fever, and pulmonary tuberculosis are liable are due to the 
action of the streptococcus in the body rendered unusually vulnerable 
by the existence of another form of infection. 

Streptococci which upon their isolation from the body in suppur- 
ative or other infectious processes are very virulent, usually, and 
sometimes very quickly, partially or wholly lose this virulence under 
artificial cultivation. 

On the other hand, cultures of streptococci which have largely 
lost virulence under artificial cultivation, or whose initial virulence 
was slight, may experience a great exaltation of virulence by a long- 
succession of inoculations from animal to animal. 

The metabolic products formed by virulent streptococci growing 
in nutrient broth, when freed from the germs by filtration, have been 
found to cause in animals the symptoms of toxaemia. The results of 

1 For an exhaustive review of suppurative inflammation from the modern stand- 
point with bibliography consult Janowski, Ziegler's Beitrage zur path. Anatomie, 
etc., Bd. xv., p. 128, 1894. 

For a table showing relative frequency of different forms of pyogenic bacteria 
in one hundred and thirty-five surgical cases in New York, consult Dowd, New York 
Medical Record, September 8th, 1894. 



THE INFECTIOUS DISEASES. 193 

preliminary experiments on immunization with these toxic products 
of Streptococcus pyogenes and the use of the blood serum of the 
immune animal for therapeutic purposes appear to be promising. But 
the details of preparation and the practical value of the so-called strep- 
tococcus antitoxin are at this date not fully determined. 

Other forms of bacteria than the "pyogenic cocci" may incite 
suppurative inflammation. Thus the pneumococcus, the typhoid 
bacillus, and the tubercle bacillus not infrequently, in addition to 
their more common and characteristic action in the body, set up com- 
plicating suppurations. Several other forms of germs have been 
found in suppurative inflammation, among which we need onlv men- 
tion here: Staphylococcus gilvus; Staphylococcus pyogenes citreus; 
Staphylococcus salivarius pyogenes; Staphylococcus cereus albus and 
flavus; Micrococcus tetragenus; Bacillus coli communis; Bacillus 
pyogenes fcetidus; Bacillus pyocyaneus; Diplobacillus pneumoniae 
(Friedlander) ; Bacillus proteus; Bacillus aerogenes capsul a tus; Bacil- 
lus pyogenes soli (Bolton) ;' Bacillus pyogenes flliformis (Flexner). 2 

The bacteria which are found in the various phases of suppurative 
inflammation may lie free in the interstices of the tissue with the 
exudate, or they may be in part within the cells which have gathered 
(see Fig. 69). 

1 Bolton, American Journal of the Medical Sciences, June, 1892. 

2 Flexner, The Journal of Experimental Medicine, vol. i., p. 211, 1896. 



ERYSIPELAS. 

Erysipelas is a diffuse inflammation of the skin and subcuta- 
neous tissue which tends to spread, and which especially involves the 
lymph spaces and the lymph vessels. It is characterized locally by 
swelling of the tissue and a bright-red color of the integument. It 
is regularly accompanied by constitutional disturbances, the most 
marked of which is fever. The morphological changes at the seat 
of lesion, as we see them after death, vary considerably in different 
cases and in different stages of the disease. The redness of the 
disease usually disappears after death. But the tissues may be 
swollen by the accumulation of serous fluid. This fluid may be 




~ r ■ ^TU(i<ker["* 



Fig. 72.— Erysipelas of the Skin. 
Showing streptococci in the lymph spaces. 



nearly transparent, or turbid from admixture with pus cells. Pus 
cells may infiltrate the tissues either sparsely or in dense masses. 
Sometimes vesicles are found on the surface, or scabs; sometimes 
more or less of the affected region becomes filled with abscesses or 
gangrenous. In some cases we find, aside from the local lesions, 
petechiae in the serous membranes, swelling of the spleen, and paren- 
chymatous degeneration of the kidneys and liver. 

The researches of Fehleisen and others have shown that erj^sipelas 
is caused by the presence and action in the tissues of a chain coccus 
(Fig. 72) called Streptococcus erysipelatis. These bacteria are 
usually most abundant in the lymph vessels and lymph spaces along 



THE INFECTIOUS DISEASES. 



195 



the advancing borders of the inflammatory area, but they may be 
contained in the blood vessels (see Fig. 73). 

In its morphological and biological characters the so-called Strep- 
tococcus erysipelatis appears to be identical with the Streptococcus 
pyogenes. 

Subcutaneous inoculation of rabbits with the pure culture may 
induce a fairly typical erysipelatous inflammation, but, as these 
animals are not especially susceptible to its action, the results of in- 
oculations are not constant. 

There appears to be good reason for the belief that many forms of 
simple phlegmonous and other exudative inflammation, and many if 
not all forms of erysipelas, are different phases of the inflammatory 




Fig. 73. —Streptococci in Masses in the Blood and Lymph Vessels of the Skin in Erysipelas. 



process due to the same organism ; the difference in the reaction of 
the tissues which in the main constitute the clinical differences char- 
acteristic of the different diseases being due> perhaps to differences 
in the tissues involved, perhaps to variations in the characters and 
virulence of the germ, and perhaps to causes which at present we 
know nothing about. 

Further researches are required to explain fully the exact relation- 
ship of these at least closely allied forms of inflammation to one 
another and to the bacteria which cause them. 

In the mean time it should be borne in mind that in the use of such 
names as Streptococcus erysipelatis one intends to express simply the 
source of the germ rather than to convey an implication of specific 
character, or of essential variation from the common Streptococcus 
pyogenes. 



SEPTICAEMIA AND PYEMIA. 

It has long been known that a certain number of persons who 
have received injuries or wounds, by accident, in childbirth, or far 
less frequently than formerly by the hands of the surgeon, may suffer 
from constitutional s} 7 mptoms and develop local or disseminated 
lesions. To designate the condition of these patients the terms pyaemia, 
septicaemia, septico-pyaemia, pyo-septicaemia, ichoraemia, inflamma- 
tory fever, surgical fever, traumatic fever, suppurative fever, and 
purulent infection have been used. Attempts to distinguish these 
several forms of disease have not hitherto proved very satisfactory, 
because the causes of the various conditions were not definitely under- 
stood. 

Since, however, we have come to know the nature of infectious 
disease, we are able to make at least a general distinction between 
two fairly typical phases of infection which have long been recog- 
nized. 

If from a focus of suppurative inflammation due to micro-organ- 
isms, or if from a point of entrance of micro-organisms without local 
reaction, the germs and their products become distributed through 
the body, inducing disease, the general condition is called septiccemia. 

If in the invasion of the body by the micro-organisms and their 
products new suppurative foci be established, it is now customary to 
designate the condition as pycemia. 

The term pyaemia then indicates a clinical and anatomical phase 
of septicaemia, and the relationship of the two conditions is frequently 
expressed by the term septico-pyaemia or pyo-septicaemia. 1 

The new foci of suppuration in pyaemia are called metastatic 
abscesses, and in distribution these may bear an obvious relationship 
to the seat of the primary lesion. Thus in suppurative processes in 
the intestinal tract metastatic abscesses are liable to occur in the 
liver. From suppurations in the skin, bones, muscles, .etc., infec- 
tious emboli may be transmitted to the lungs, causing infarctions and 
abscess ; or, passing these organs, the germs may induce multiple 
abscesses in the kidneys and in other viscera. 

1 The word pyaemia was originally framed to express the conception that the in- 
vasion of the blood by pus cells was the significant thing in this condition. This 
conception we now know to be incorrect. 



THE INFECTIOUS DISEASES. 



197 



It should also be remembered that the point of introduction into 
the bod} T of the offending germs may be wholly concealed and not 
associated with any form of demonstrable external lesion. This is 
often called cryptogenetic pyaemia or septico-pyaemia. 

While septicaemia and pyaemia are most commonly due to the 
presence and growth and distribution in the body of the pyogenic 
staphylococci and streptococci, these phases of infection are not infre- 
quently associated with the pneumococcus, gonococcus, the typhoid 
bacillus, the anthrax bacillus, the colon bacillus, certain gas-forming 
bacilli, and various other germs. 1 

Finally, the possibility should not be lost sight of here that under 
certain little understood conditions toxic materials may be elaborated 




Fig. 74.— Micrococci in Masses in the Fibrinous Exudation of Pyemic Pleurisy. 



by the body cells themselves, which may give rise to some of the 
phenomena of septic poisoning. 

The varying phases of so-called puerperal fever are to be classed 
under the heading of septicaemia or pyaemia, and it is unusually 
caused by the Streptococcus pyogenes. 2 

After death from septicaemia and pyaemia there is a considerable 
variety in the post-mortem appearances. 

1. There are cases in which there are no recognizable lesions. 

2. There are cases characterized by early post-mortem decomposi- 

1 Canon, "Bakteriol. Blutunters. bei Sepsis," Deutsche med. Wochenschrift, 
October 26th, 1893. p. 1038. Consult also Petruschky, Zeitschrift f. Hygiene, Bd. 
xvii., pp. 59 and 109, for methods of detection of bacteria in the blood of septicaemia. 

-Consult Goldscheider, "Klin. u. Bak. Mitth. u. Sepsis Puerperalis, " Charite- 
Annalen, Jahrgang 18, p. 237. 



198 THE INFECTIOUS DISEASES. 

tion; post-mortem staining of the tissues; congestion of the lungs, 
stomach, intestines, and kidneys; extravasations of blood in the 
serous membranes; swelling of the solitary and agminated lymph 
nodules in the small intestine; swelling of the spleen and parenchy- 
matous degeneration of the liver and kidneys. 

3. In some cases there are localized inflammations. The joints, 
the connective tissue around the joints, the pleura (Fig. 74), 
the pericardium, the peritoneum, the pia mater, and the connective 
tissue in different parts of the body may be inflamed. These local 
inflammations are of a purulent character, except in the serous mem- 
branes, where the principal inflammatory product may be fibrin. 

4 . There are cases in which the veins in the neighborhood of the 
wound contain softened, puriform thrombi; without infarctions in 
the viscera, there may be inflammation of the joints and serous mem- 
branes. 

5. In other cases the veins contain thrombi; there are infarctions 
and abscesses in the viscera; local inflammations of the joints and 
serous membranes may be present or absent. The thrombi are 
formed regularly in the veins near the wound, but they may be sit- 
uated in veins at a distance, and sometimes, although infarctions and 
abscesses are present, jio thrombus can be discovered. The veins 
may be distended by the thrombi or only contain small coagula. 
The different kinds of thrombi, and the varieties of emboli and in- 
farctions which they produce, are described in the article on Throm- 
bosis, page 72. 

Various lines of research on minute changes in cells which bac- 
terial and other poisons may induce justify the expectation that more 
and more we shall be able to associate characteristic groups of symp- 
toms in septicaemia, for which there is now no morphological basis, 
with well-defined cell alterations. 



ACUTE CEREBROSPINAL MENINGITIS. 

This is usually defined as an acute infectious disease of which the 
characteristic lesion is an exudative inflammation of the pia mater 
of the brain and cord. It may, however, be regarded as an infec- 
tious inflammation of the pia mater accompanied by constitutional 
symptoms. At ail events, there are inflammations of these mem- 
branes, which occur both as isolated cases and also in epidemics, with 
similar symptoms and similar lesions, and which are not apparently 
caused by traumatism nor by infection from other foci of inflamma- 
tion. 

As a rule the inflammation of the pia mater results in a large pro- 
duction of serum, fibrin, and pus, which infiltrate the pia mater and 
accumulate in the ventricles, so that the gross appearance of the 
brain is characteristic. The exudation is especially abundant at the 
base of the brain and over the posterior surfaces of the cord. In 
children the distention of the lateral ventricles with purulent serum 
may be a marked feature, while in adults the quantity of serum is 
apt to be small. 

It is important to remember that a meningitis which induces 
marked cerebral symptoms, continues for a number of days, and 
causes death, may produce so little change in the pia mater that after 
death this membrane upon gross examination looks normal. This is 
especially common when the disease is not epidemic, but occurs in the 
sporadic form. 

When, however, we look at the pia mater in these cases with the 
microscope we find a slight infiltration with pus and fibrin, or a 
growth of new cells resembling the cells of the pia mater. 

While the above are the characteristic lesions of this disease, 
there are a number of secondary or associated changes in different 
parts of the body which are not constant, but which occur with suffi- 
cient frequency to render their mention necessary. There may be 
subserous punctate haemorrhages in the endocardium; petechise in 
the skin ; hyalin and granular degeneration in the voluntary striated 
muscle; occasional multiple abscesses in various parts of the body; 
suppurative inflammation of the joints; parenchymatous degenera- 
tion of the heart, liver, and kidneys; and swelling of the gastro- 
intestinal lymphatic apparatus and of the spleen. 



200 THE INFECTIOUS DISEASES. 

Cerebrospinal meningitis may occur by itself or in connection 
with some other acute infectious disease, such as acute lobar pneu- 
monia, mycotic ulcerative endocarditis, pyseniia, multiple suppura- 
tive arthritis, otitis media, puerperal fever, typhoid fever, etc. 

The lesions are essentially the same in epidemic and in sporadic 
cases of acute cerebro-spinal meningitis, and. in both modes of occur- 
rence the disease is probably caused by bacteria. 

Numerous careful studies have been made on the bacteria occur- 
ring at the seat of lesion in sporadic cases occurring both with anc 
without complicating lesions in other parts of the body. 

The Streptococcus pyogenes has been demonstrated in a few cases. 
occurring in connection with suppurative inflammations elsewhere. 

The Diplococcus lanceolatus (pneumococcus) (see page 201) has 
been found in several cases, and in some of these without any lung 
lesion. Weichselbaum has described the occurrence in several cases 
of a diplococcus not known to occur elsewhere, which was founc 
largely confined to the pus cells,. and which he called Diplococciu 
intracellular is meningitidis. Animal experiments with this as wel 
as the pneumococcus would indicate that they may stand in a cau- 
sative relation to the disease. Some other scattering forms of bacterig 
have been described, but not with sufficient frequency and definitive- 
ness to enable us to judge of their significance. 

It seems probable, therefore, from what we know at present, thai 
several forms of bacteria are capable of causing acute cerebro-spina' 
meningitis. Which is the most frequent and important, it remains 
for further researches to show. 

Bacterial studies of the cases in epidemics of cerebro-spina] 
meningitis have not been numerous since the development of the 
new technique. But there is reason to believe that the Diplococcus 
lanceolatus plays here also an important role. 1 

The close topographical relationships which the nasal cavities and 
the middle ear bear to the meninges is significant in this connection 
on account of the possibility of the transmission to the brain mem- 
branes of bacteria not uncommonly present and usually harmless in 
the former situations, 

1 For literature and a study of cases consult article on "Epidemic Cerebro- Spinal 
Meningitis, " by Flexnerand Barker, American Journal of the Medical Sciences, 1894. 
Also Jliyer, Zeitschrift f . Hygiene, etc., Bd. xix., p. 351. 



ACUTE LOBAR PNEUMONIA AND OTHER INFECTIOUS 

DISEASES INDUCED BY THE DIPLOCOCCUS 

LANCEOLATUS. 

(Pneumococcus : Diplococcus pneumoniae.) 

This germ is frequently spoken of as the pneumococcus of 
Frankel, because its significance and life history in connection with 
acute lobar pneumonia were first demonstrated by him. 1 During 
their development these germs are distinctly spheroidal. But in 
their mature condition they are apt to become slightly elongated and 
often a little broader at one end than at the other, assuming a lanceo- 
late form. They are very apt to occur in pairs, and frequently are 
seen in short chains, rarely in long chains. Very frequently, when 



• v 



Fig. 75.— Diplococcus Lanceolatus (Pneumococcus) with Capsules. 
Stained by Welch's method. 

growing in the living animals, the pneumococcus is surrounded by a 
distinct, homogeneous capsule of varying thickness (see Fig. 75). 
This capsule does not, as a rule, develop in artificial cultures. The 
coccus itself is readily stained ; the capsule is not easily demonstrated 
except by special staining methods. 

The pneumococcus has no spontaneous movement and grows but 
feebly at ordinary room temperature. It grows much better at the 
temperature of the body, forming on the surface of very slightly 
alkaline agar 2 plates faint grayish, dewdrop-like, inconspicuous 

1 It was discovered by Sternberg in saliva, and its pathogenic power demon- 
strated, some years before its full significance was understood in connection with 
pneumonia. 

2 The growth of the pneumococcus is less certain and abundant on the ordinary 
agar than on Guarnieri's gelatin agar mixture or on Welch's modification of this. 
The formula for this modification is : 950 gm. meat infusion, 5-10 gm. pepton, 6-8 
gm. agar, 30-40 gm. gelatin. The gelatin and agar are boiled separately in 50 

17 



202 THE INFECTIOUS DISEASES. 

colonies, somewhat similar to those of Streptococcus pyogenes, bul 
usually more delicate. In beef tea it forms at body temperature a 
faint whitish sediment with slight turbidity of the fluid. As a rule, 
the cultures are prone to soon lose their virulence and to die off early, 
but the virulence may be maintained by successive inoculations in 
the rabbit. 

The pneumococcus injected, while virulent, subcutaneously ink 
mice and rabbits induces a rapidly fatal septicaemia, often with little 
marked anatomical change, save enlargement of the spleen. Some- 
times there are necrotic foci in the liver, fibrin in the glomeruli oi 
the kidneys, fatty degeneration of the heart. Suppurative inflam- 
mation at the seat of inoculation and elsewhere may follow. The 
blood and viscera may show under these conditions numerous cocci, 
mostly with capsules, or they may be confined to the seat of inocula- 
tion. Cultures which have been reduced in virulence, so as not tc 
cause early death by septicaemia, may, when introduced into the 
trachea of rabbits, induce a fairly typical lobar pneumonia. 

Different species of animals show marked differences in vulner- 
ability to the ravages of the pneumococcus. This germ is the exclu- 
sive inciter of typical acute lobar pneumonia in man. It appears tc 
act, in part at least, by the development of an albuminous poison 
which has been tentatively called pneumotoxin. It would seem tc 
be the pneumotoxin which induces the symptoms in acute lobai 
pneumonia indicative of systemic poisoning, since the bacteria them- 
selves are usually confined to the lungs. 1 

For a more detailed description of these lesions of pneumonia, and 
an account of other bacteria which may be present, see page 438. 

In addition to its more common effect in inducing lobar pneu- 
monia, this diplococcus has been very frequently found in, and 
stands apparently in a causative relation to, some forms of exudative 
inflammation of the serous membranes, either in connection with oi 
without a primary lobar pneumonia. Thus it has been repeatedly 
found in pleuritis, otitis, meningitis, empyaema, pericarditis, endo- 

— . . 

c.c. of water before mixing. The reaction should be made distinctly but feeblj 
alkalin. The mixture solidifies at room temperature. It should be used in Petri 
plates, and though it softens the colonies remain separate at 35° C. (see Johns 
Hopkins Hospital Bulletin, December, 1892). It is especially important in pre- 
paring culture media for the pneumococcus to use the most exact tests available foi 
fixing the reaction, since the vigor of the growth is, as T. C. Janeway has shown, 
closely dependent upon this. 

1 The observations of the Klemperers suggest the possibility that at a certain 
period of the disease the blood or body juices are capable of developing a substance 
antidotal to this pneumotoxin, the advent of the former being signalized by the 
so-called "crisis. " Satisfactory applications of this alleged "pneumonia antitoxin' 
in therapeutics have not yet been made. 



THE INFECTIOUS DISEASES. 203 

carditis, and in peritonitis. It has also been found in abscesses of 
the viscera and in exudative inflammation of the joint. 

The Diplococcus lanceolatus is a frequent inhabitant of the mouth, 
even in health. It has been found in the mouths of about twenty per 
cent of healthy persons examined. It is thrown off in the sputum in 
lobar pneumonia, and no doubt from these sources in the dried condi- 
tion, as dust, furnishes the infectious agent which in favoring con- 
ditions of the body lights up the inflammatory process in the lungs. 

For staining the pneumococcus with its capsule the method suggested by Welch 1 
gives the most satisfactory result. 

The exudate containing the germ is dried and fixed upon the cover glass in the 
manner described on page 154. It is now treated with glacial acetic acid, which is at 
once drained off and replaced by anilin-gentian-violet solution (page 156) this being 
drained off and renewed several times until the acetic acid is displaced. The speci- 
men is now washed with a two-per-cent solution of sodium chlorid, in which it may 
be covered and studied. 

Such specimens are not usually suited for permanent preservation, although 
occasionally after drying and mounting in balsam the capsules retain their color. 
Annoying color precipitates frequently interfere with full success by this method. 

The pneumococcus may be stained in sections by Weigert's modifications of 
Gram's method with preliminary contrast stain (see page 157). By this method the 
fibrin in the pneumonic exudate is also stained. 

1 Welch, Johns Hopkins Hospital Bulletin, December, 1892, p. 128. 



INFECTIOUS PSEUDO-MEMBRANOUS INFLAMMATION 

OF MUCOUS MEMBRANES. 
> 

(Pseudo-Diphtheria : Diphtheroid- Angina ; Membranous 

Angina.) 

Under a variety of conditions, as during scarlatina and measles 
whooping-cough, typhoid fever, etc., or entirely apart from an\ 
complicating disorder, an acute exudative inflammation of the mu 
cous membranes, especially of the upper air passages, occurs, whicl 




Fig. 76.— Pseudo-membranous Inflammation op Trachea. 
In this case there is purulent infiltration of the mucosa and submucosa, and of portions of th 
mucous glands, a, false membrane; &, portion of intact epithelium; c, infiltration of the mucos; 
with fibrin; d, portion of mucous gland infiltrated with pus. 



is associated with, and is apparently caused by, the growth o 
a streptococcus (Fig. 77) which in morphological and biologica 
characters seems to be identical with the Streptococcus pyogenes 
There may be much or little fibrinous exudate; there may in earh 
stages, or even throughout, be none at all. The pellicle when forme< 
may be loose or adherent, sharply circumscribed or tending to spread 
The submucous tissue may show little change, or may be congeste< 



THE INFECTIOUS DISEASES. 



205 



and cedematous, or may be the seat of suppurative inflammation 
(see Fig. ?6), necrosis, or gangrene. The process may be confined to 
the tonsils. While under these varying conditions the inflammatory 
process is usually a local one and runs its course with or without the 
symptoms of septicaemia, occasionally the streptococcus finds access 
to the blood and may induce the lesions of pyaemia. On the other 
hand, it may by aspiration gain access to the lungs and induce 
varying phases of complicating broncho-pneumonia. The Staphylo- 
coccus pyogenes is not infrequently associated with the streptococcus 
in these lesions, but is not apparently of primary significance. Sim- 






5«^3? 








Fig. 77. —Infectious Croupous Ijtflamiiation of the Trachea. 
Section through the pseudo -membrane and underlying tissue, showing large numbers of strep- 
tococci. 

ulating very closely, as it does in many cases, both the local and 
general phenomena of diphtheria, this disorder has formerly been 
confounded with it, and has been only recently recognized as a distinct 
phase of disease. It is now most frequently called pseudo-diphtheria. 
It seems in part to cover the condition formerly known as croup, in 
part those cases formerly thought to be mild diphtheria. 1 In many 
phases of acute angina, in many cases of follicular tonsillitis, strepto- 
cocci have been found in large numbers. 

1 For a general consideration of the relationship between this form of pseudo- 
membranous inflammation and diphtheria, with original studies and bibliography, 
consult Park, "Diphtheria and Allied Pseudo-Membranous Inflammations, " Medical 
Record, July 30th and August 6th, 1892. 



GONORRHOEA AND OTHER INFLAMMATORY LESIONS 
INDUCED BY THE MICROCOCCUS GONORRHCE^E 

(GONOCOCCUS). 

The Micrococcus gonorrhoeae is most commonly found in the 
exudate of gonorrhceal inflammation of the mucous membranes, 
especially of the urethra. It may be found free or enclosed in leu- 
cocytes or other cells within or between the superficial epithelial cells. 
It is also often present in the exudate in arthritis, and in tubal, ova- 
rian, perimetritic, and other inflammations, arising as complications 
of gonorrhoea. 

Under these complicating conditions the gonococcus may occur 
alone or in association with the pyogenic cocci. It is generally most 
abundant during the acute stage of the inflammation. 

The gonococcus is apt to occur in pairs, the apposed sides being 
more or less distinctly flattened (Fig. 78) . It stains readily with the 






Fig. 78. —Micrococcus Gonorrhea (Gonococcus). 

anilin dyes, and differs from most known cocci which might be 
mistaken for it in that it is decolorized by the iodin solution in the 
Gram's method of staining. 

If after the use of the iodin solution in Gram's method the cover 
glass be rinsed with alcohol to complete the decolor ization and then 
with water, and the specimen be stained for a few minutes in a dilute 
aqueous solution of Bismark brown, rinsed and mounted in balsam, 
the gonococci will appear of light-brown color, while most other 
germs will retain the violet color (see Fig. 79). In exudates a con- 
siderable part of the gonococci are usually contained in the bodies of 
pus cells. 

The gonococcus thrives best at about the temperature of the body 
(37° C.), and has been artificially grown on a variety of culture media 
which contain considerable albuminous material in solution. Human 



THE INFECTIOUS DISEASES. 



207 



blood serum — squeezed from the placenta — and mixed with pepton- 
ized agar in accordance with the method of Wertheim, has been in 
the past most commonly employed for cultures. 

Heiman 1 has found the clear exudate or transudate from the 
pleural cavities in man (" chest serum") to form a convenient and ex- 



FlG. 




A. Cover Glass Preparation of Goxorrhceal Exudate. 



Stained by Gram's method with gentian violet; contrast stain with Bismark brown. The 
gonococci have been decolorized by the iodine solution and restained by the brown: while other 
bacteria cocci and bacilli which were mingled with them still retain the original violet color. 



cellent substitute for blood serum. This is sterilized by the discontin- 
uous or fractional method 2 (or it may be filtered through an unglazed 
porcelain filter), and then mixed with two-per-cent agar — containing 




Fig. 80.— Pes Cells containing Goxococci. From a case of gonorrhceal urethritis. 

one-per-cent pepton and one-half -per-cent salt — in the proportion of 
one part of the serum with two parts agar, melted at about 40° C. 

1 Heiman, "A Clinical and Bacteriological Study of the Gonococcus, " etc. Xew 
Fork Medical Record, June 22d, 1895, contains bibliography. 

2 In fractional or discontinuous sterilization, the serum, filled into tubes, is exposed 
for an hour on five successive days to a temperature of from 65° to 68° C, standing 
in the interval at the ordinary temperature of the room. In this way the serum may 
be rendered sterile 'without coagulation, which seriously interferes with its value as 
a culture medium for the gonococcus. 



208 THE INFECTIOUS DISEASES. 

In this chest-serum agar the surface growth of the gonococcus is in 
the form of small circular, sharp-edged, slightly raised, grayish-white 
colonies, coarsely mottled in the central portion, finely granular 
toward the borders. The lower animals are not, as a rule, susceptible 
to inoculations of the mucous membranes with the gonococcus, but 
suppurative inflammation has been induced in mice and guinea-pigs 
by intraperitoneal injections. Inoculations of pure cultures of the 
gonococcus upon the urethral mucous membranes of man is followed 
by a characteristic catarrhal inflammation. 

The evidence is now complete that the gonococcus stands in a 
causative relationship to the characteristic inflammation with which 
it is so constantly associated. 

But in what measure this germ, in what measure the strepto- 
coccus and staphylococcus may be responsible for the complicating 
inflammations when both germs occur together, is yet to be deter- 
mined. Inasmuch as one or more forms of cocci and diplococci 
occurring in the normal and in the inflamed urethra are morphologi- 
cally similar to the gonococcus, great caution should be exercised in 
doubtful cases in pronouncing upon the nature of suspicious germs. 
But the pronounced tendency of the gonococcus to gather within cells; 
the sometimes conspicuous but often ill-defined flattening of the 
apposed sides of the gonococci; the decolorization by Gram's method, 
which leaves most other germs apt to be associated with the gono- 
coccus still stained, and whenever practicable the artificial culture 
characters — these all should be considered in the summary of evi- 
dence. [ 

1 Von HiUer, Centralbl. f. Bakteriologie, etc., Bd. xix., p. 120, 1896. For sum- 
mary of current work on the gonococcus with bibliography consult Neisser and 
Scliaffer, " Ergebnisse der allg. Aetiologie der Menschen- u. Thierkrankheiten, " 1896, 
p. 477. 



ANTHRAX. 
{Splenic Fever; Malignant Pustule; Charbon; Carbuncle.) 

This disease, which is much more common in the lower animals, 
especially the herbivora, than in man, is widely prevalent in Europe. 
It is rare in the United States, but seems in certain regions to be 
more common than formerly. 

It is induced in man by accidental inoculation with the Bacillus 
anthracis, which causes the disease in the lower animals. Inocula- 
tion may occur through the skin by the agency of flies and other 
insects which have been feeding on animals infected with this disease; 
by handling their carcasses or hides, or in other ways. Following 




Fig. 81.— Anthrax— Malignant Pustule— of the Skin. 
From a man in New York who had been handling foreign hides. Bacilli stained with gentian 
"violet. 

this skin inoculation a pustule is apt to develop — " malignant pustule" 
— and varying phases of an acute exudative inflammation, which may 
be hsemorrhagic, sero-fibrinous, purulent, or necrotic, accompany the 
local proliferation of the germs (Fig. 81). From this local source a 
general infection may ensue. In some cases general infection may 
occur without evident external lesion. 

Infection with anthrax may occur through the lungs, most often 
among those who handle infected wool or hides, the dust from which 
is inhaled ("wool-sorter's disease"). Under these conditions there 
may be oedema, lobular pneumonia with involvement of the pleura, 






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212 THE INFECTIOUS DISEASES. 

By inoculation of animals with anthrax cultures, beginning wit 
those which, having been maintained at 42° C. for from fifteen 1 
twenty days, and thus possessing but feeble virulence, and passin 
to those cultivated at 42° C. for a shorter time and which were therefoi 
more virulent, Pasteur was able to secure immunity from anthra 
in a series of the lower animals. Based upon these experiments 
method of protective vaccination has been practised on a large seal 
among sheep and other animals in some parts of Europe and has bee 
of great economic value. According to some authorities the deat 
rate from anthrax has under these preventive inoculations been reduce 
in sheep from ten per cent to about nine-tenths of one per cent, an 
in cattle from five per cent to less than four-tenths of one per cent. 



TUBERCULOSIS. 

Tuberculosis is an infectious disease characterized by inflammatory 
and necrotic processes in the body due to the presence and growth of 
the Bacillus tuberculosis (tubercle bacillus). The most distinctive 
morphological feature of tuberculosis is the development under the 
influence of the tubercle bacillus of larger and smaller gray or white 
or yellow, firm or friable masses of tissue called tubercles. 

The Bacillus tuberculosis is a long, slender bacterium varying in 
length from 3 to 4 fi (from one-quarter to one-half the diameter of a 
red blood cell) and in breadth from 0.2 to 0.5 /*. It is frequently 






'\J\ 




' 



Fig. 84.— Tubercle Bacilli m Sputum from a case of Pulmonary Tuberculosis, 
Showing the bacilli in pus cells. 

more or less curved, and the individual bacilli may cling together end 
to end, forming threads or chains. The bacillus (Fig. 84) is stained 
with difficulty by the anilin dyes (see below) , and when stained often 
presents an irregular beaded or knobbed appearance, due to an un- 
evenness in the coloring of the protoplasm, or to involution changes. 
It is immobile and spores have not been demonstrated in it. 

At the temperature of the body it can be grown on many of the 
artificial culture media, such as coagulated blood serum, five-per-cent 
glycerin -agar, five-per-cent glycerin-nutrient broth, on potato, and 
in a variety of organic and inorganic mixtures. 



214 



THE INFECTIOUS DISEASES. 



The growth of the tubercle bacillus in cultures is very slow in 
comparison with that of most of the pathogenic micro-organisms. 
After several weeks' growth it forms dry, scaly masses or thin, 
wrinkled pellicles on the surface of the media (Figs. 85 and 86) . 

It requires a certain amount of oxygen for its growth, and thrives 
best in the dark. It is killed by an exposure of a few hours to direct 









Fig. 85. 



Fig. 86. 



Fig. 85.— Culture of Tubercle Bacillus on Glycerin Agar. — From tuberculosis in the bird. 
Fig. 86.— Culture of Tubercle Bacillus on Glycerin Agar.— From tuberculosis in man. 



sunlight, or if moist is killed by an exposure of from ten to fifteen 
minutes to 70° C. On the other hand, it may long retain its vitality 
in the dried condition. 

Cultures can be continued indefinitely from generation to genera- 
tion with a slowly diminishing virulence which finally is largely 
lost. Under certain conditions the virulence may be restored or 
enhanced by successive inoculations into susceptible animals. Certain 
modified forms or varieties or races of the tubercle bacillus are 



THE INFECTIOUS DISEASES. 215 

known, notably that which is concerned in inducing the lesions of 
fowl tuberculosis. 

The tubercle bacillus does not, so far as we know, grow in nature 
outside of the bodies of men and certain warm-blooded animals. It 
is thus strictly parasitic. 

Tuberculosis is a very common disease not only of man but also 
of many of the lower animals, especially of cattle, and inasmuch as 
the victims of this disease, both men and animals, are apt to throw off 
enormous numbers of the bacilli in the sputum and other excreta, the 
germ is very widely dispersed in inhabited regions, especially in 
buildings frequented by uncleanly tuberculous persons or by infected 
cattle. It may be conveyed by the milk and milk products of tuber- 
culous cows. 

Among the lower animals, guinea-pigs, rabbits, monkeys in con- 
finement, and cattle are particularly susceptible to the action of the 
tubercle bacillus. Although tuberculosis is widespread in man, he 
is not, as compared with some of the lower animals, particularly sus 
ceptible. While the tuberculous process presents some special dif- 
ferences indifferent animal species in rate of development, amount of 
necrosis, tendency to softening, calcification, etc., the fundamental 
effects are similar in man and in the lower animals. 

The effect on the bod}' cells of the presence and growth of the 
tubercle bacillus varies considerably, depending upon the number and 
virulence of the germs present, the character of the tissue in which 
they lodge, and the vulnerability of the individual. In general, it 
may be said that tubercle bacilli may stimulate the connective-tissue 
cells in their vicinity to proliferation ; or they may excite emigration 
of leucocytes from blood vessels and lead to the production of other 
exudates; or they may cause death of tissue. Thus the phases of 
inflammation which are excited by the tubercle bacillus are produc- 
tive, exudative, and necrotic. The tubercle bacillus may produce 
these effects separately or simultaneously, in the sequence just indi- 
cated or in some other ; and now one, now another of them may pre- 
ponderate. 

Tuberculosis manifests itself most often in the form of an inflam- 
mation affecting some one part of the body, as the lungs (the part 
most frequently involved in adults), the gastro-intestinal tract or 
the skin — "localized tuberculosis." While the lungs are most 
frequently involved in tuberculosis in adults, in children it is the 
lymph nodes which are most commonly affected, 1 and very often the 
bones and joints. Such a localized tuberculosis ma}" retain through- 
out the characters of a local inflammation, or it may be accompanied 
by the clinical evidences of systemic infection. It may give rise 
1 See yortlirup, New York Medical Journal, February 21st, 1891. 



216 THE INFECTIOUS DISEASES. 

through metastasis to the successive development of tuberculou 
inflammation in other parts of the body, or to a sudden developmen 
of tuberculous inflammations in many parts of the body at the sam< 
time — general miliary tuberculosis. 

A general infection may be caused by the diffusion through th 
body of bacilli derived, from a local tuberculosis, such as tubercula 
phlebitis or arteritis, or from the breaking into a vessel of a tuber 
culous lymph node, or by the inspiration into the lungs of larg< 
numbers of bacilli. 

In a considerable proportion of cases the local lesions produced \r 






Fig. 87.— A Miliary Tubercle from a Lymph Node, x 850 and reduced. 
The giant cells are enclosed by the basement substance. 

the tubercle bacillus are in the form of circumscribed nodules o 
masses of new -formed cells or tissues which are called tubercles, o 
if small miliary tubercles. 

In many cases, however, the lesion is not circumscribed bu 
diffuse, and more or less widely infiltrates or replaces the tissue 
involved. This is called diffuse tuberculous inflammation (dif 
fuse tubercle). 

Miliary Tubercles. — Miliary tubercles are small nodules of irreg 
ularly spheroidal shape (Figs. 87, 88, 90, 223 and 224), the smalles 



THE INFECTIOUS DISEASES. 



217 



hardly visible to the naked eye, the largest as large as a pea. 1 The 
smaller tubercles are gray and translucent; the larger are usually, 
especially in the central parts, opaque and white or yellow on account 
of the necrosis which is apt to commence here. 

In studying the effects caused by the tubercle bacillus on living 
tissues it should be always borne in mind that while as a whole the 
lesions produced are quite characteristic, there is still no one structural 
feature or combination of features of tubercles or tuberculous inflam- 
mation which is absolutely distinctive of the action of this germ. In 




Fig. 88.— A Miliary Tubercle from the Pleura. X 850 and reduced. 
The branches of the giant cells form part of the basement substance. 

doubtful cases the demonstration of the presence of the germ itself 
may be necessary for the establishment of the character of the lesion. 2 

1 The term miliary tubercle, which arose from the crude coincidence in size be- 
tween small foci of tuberculous inflammation and some forms of millet seed, is now 
very liberally applied to tubercles which are very much larger as well as to those 
which are very much smaller than millet seeds. It is convenient to designate a 
spheroidal mass of new tissue formed under the influence of the tubercle bacillus, 
whatever its minute structure, as a tubercle granulum (see Fig. 188) . Very fre- 
quently two or more tubercle granula are joined together by a more diffuse forma- 
tion of tubercle tissue to form larger or smaller miliary tubercles — conglomerate tuber- 
cles (see Fig. 189) . 

2 The term tubercle tissue, which is in common use, indicates a tissue formed 

18 



218 



THE INFECTIOUS DISEASES. 



The experimental studies in animals, as well as the morphologica 
data gathered from the examination of tuberculosis in man, show thai 
when tubercle bacilli in moderate numbers lodge and develop in th( 
living body one of the early local effects is a proliferation of the con' 
nective tissue and endothelial cells. These become larger and poly 
hedral, with conspicuous nuclei. These new cells are often callec 
epithelioid on account of their approach in form to the epithelia 
cell type (Fig. 87). 

A new reticulum or stroma may form hand-in-hand with th< 




Fig. 89.— Tuberculous Tissue. Showing giant cells. Photograph from a miliary tubercle. 



growth of these new cells (Fig. 88), or the old stroma may persist 
adapting itself in form and arrangement to the new conditions. 

Either after the connective-tissue cell proliferation or hand-in 
hand with it, or preceding it, or altogether independently of it, emi 
gration of leucocytes and extravasation of serum may take place fron 
blood vessels in the vicinity of the germs. During the more or les* 
active cell proliferation which occurs under the stimulus of th< 
tubercle bacillus multinuclear cells 1 — giant cells — may be formec 

under the influence of the tubercle bacillus rather than a tissue which is morpho- 
logically characteristic of tuberculosis in distinction from other forms of new tissue 
1 For an account of giant cells, which are found under various conditions and an 
by no means confined to tuberculous inflammation, consult Marchand, Virchow'i 
Archiv, Bd. xciii., p. 518. 



THE INFECTIOUS DISEASES. 



219 



(Fig. 89), either by persistent nuclear division in growing proto- 
plasmic masses which do not divide into separate cells, or by the 
coalescence of the bodies of cells already formed. 

More or less new tissue with numerous small spheroidal mono- 
nuclear cells and little stroma may form in and about the tuberculous 
foci. Blood vessels are not apt to develop under the influence of the 
tubercle bacillus. Old blood vessels are, on the other hand, usually 
obliterated as the new tissue forms. 

Sooner or later the tubercle bacillus is apt to associate with its 











■-..-■-■ 






$v£^ 






M0m 



■. ■'■■ * '■^y-'mPti^vM 



Fig. 90.— A Nodule of Tuberculous Inflammation (Miliary Tubercle) in the Lung. 
Showing polyhedral cells, small cells, giant cells, and coagulation necrosis at the centre. 



stimulative a destructive action, which leads to coagulation necrosis 
in the new-formed tissue as well as in the old tissue of the infected 
region. This necrosis is more apt first to manifest itself in the 
central portions of the tuberculous foci (Fig. 90) and may progress 
outward ; the nuclei become fragmented or disappear, or fail to stain 
in the usual way, the protoplasm becomes more homogeneous, and 
cells and stroma form at last a structureless mass of tissue detritus 
which tends to disintegrate (coagulation necrosis or cheesy degenera- 
tion), forming cavities or, if on free surfaces, ulcers. 

As coagulation necrosis progresses, the tubercle masses lose the 



220 THE INFECTIOUS DISEASES. 

gray translucent appearance which in their early stages they are ap 
to present to the naked eye and become more opaque and of yellowish 
white appearance at the centres. 

Finally dense fibrous tissue may form in and about foci of tuber 
culous inflammation, encapsulating or sometimes entirely replacing 
the more characteristic new-formed structures. 

It is in this way — by the formation of connective tissue — tha 
such repair as is possible after local tuberculous inflammation, i: 
brought about. 

Before the discovery of the tubercle bacillus and while our knowl 
edge of the lesions of tuberculosis was largely limited to their mor 
phology, it was natural that much stress should be laid upon th< 
variety in structure which the nodular growths called tubercles pre 
sented, and that elaborate classifications and groupings of tubercle: 
were often deemed important. 

With an exact knowledge of the inciting cause of the new growth: 
and of the varying phases of their development in the body, the mor 
phological peculiarities of tubercles are not now to be regarded as o 
such extreme significance, since they for the most part indicat< 
simply variations in the local effect of a definite poison. These vari 
ations are due to differences in the amount and intensity of tin 
poison, to the degree of susceptibility of the individual, to the struc 
ture of the particular tissue or organ involved, and to the extent am 
variety of local complications caused b} r other agencies. 

It is, however, usually convenient and sometimes important t< 
recognize structural types in miliary tubercles. Thus they may b< 
composed wholly of small spheroidal cells — "lymphoid tubercles," o: 
of larger po^hedral cells — " epithelioid-celled tubercles" or of botl 
forms of cells together and with or without a new-formed stroma ; o: 
of any of these combinations with giant cells. Then coagulatioi 
necrosis, which may occur in tubercles of any type; development o 
new dense connective tissue; association with various phases o 
simple exudative inflammation — all of these contribute to the variety 
in the structural types of miliary tubercles. 

Diffuse Tuberculous Inflammation (Diffuse Tubercle). — 1. I: 
the infection with tubercle bacilli be extensive, or if step by step th< 
bacilli are distributed in the tissues about the primary seat of infec 
tion, considerable amounts of tubercle tissue of one or other forn 
may develop and pass into the condition of coagulation necrosis, s< 
that at length large necrotic masses, with a comparatively smal 
amount of well-defined tubercle tissue, either diffuse or in the forn 
of granula, may alone remain to indicate the character of old anc 
slowly progressive local infection. This form of lesion is found ir 
the large tuberculous masses in the brain, in the mucous membran( 



THE INFECTIOUS DISEASES. 



221 



of the bronchi, in large flat masses of the serous membranes, and in 
the diffuse, cheesy infiltration of the lymph nodes, kidneys, ureters, 
bladder, prostate, testicle, and uterus. 

These large areas of tuberculous inflammation are apt to be white 
or yellow in the central and necrotic portions, which are sometimes 
dense, compact, and hard, sometimes soft and friable. 

These areas are not infrequently surrounded by an irregular gray 
zone of tubercle tissue or by a dense fibrous tissue capsule. 

2. In marked contrast with the phase of diffuse tuberculous in- 




Fig. 91.— Miliary Tubercle lv Luxg of Child. 
Showing the Bacillus tuberculosis— stained with f uchsin— in the contents of the air vesicles and 
in their thickened walls. (The sizeof the bacilli relative to other elements is slightly exaggerated.; 

flammation just described, though often associated with it, is that in 
which the formation of inflammatory exudates is a prominent feature. 
This exudative form of tuberculous inflammation is best exemplified 
in the lungs by some of the forms of acute phthisis (see page 466) . 
The tubercle bacillus is under certain conditions markedly pyogenic 
and when it rapidly develops in the air spaces of the lungs or sud- 
denly gains access to them in large quantities pus, serum, fibrin, and 
exfoliated or proliferated epithelial cells may collect in and largely fill 
the air spaces, and then the whole new exudate and the old lung tis- 



222 



THE INFECTIOUS DISEASES. 



sue may, over larger or smaller areas, rapidly undergo coagulatior 
necrosis. 

Thus in one phase of tuberculous inflammation the intensity anc 
rapidity of the local poisoning by the bacillus do not permit of the 
formation of organized new tissue at all, but onty of exudative prod- 
ucts (Fig. 91). Less intense degrees of exudative inflammation arc 
liable to develop in the vicinity of miliary tubercles anywhere in the 
body, but especially in the lungs. 

It has been found that tubercle bacilli which have been killed by 
boiling or otherwise, when introduced into the body of the rabbit 




"V.-v 



%mMfks. 






•w- /h&>. '- : '■&'■ 



-s .«» 













L/^^<^#^ff jfep «4?* ,fe- ^ 






Fig. 



-Inflammatory Nodule (Pseudo-Tubercle) in the Liver of the Rabbit produced by 
the Intravenous Injection of Dead Tubercle Bacilli. 
Most of the dead bacilli have disintegrated, setting free the bacterial proteid peculiar to this 
germ, which has stimulated the new cell growth. A few fragments of the bacilli, however, still 
remain. 

either beneath the skin, into the serous cavities, or into the blood 
vessels and the air spaces of the lungs, are capable, as they slowly 
disintegrate, of stimulating the cells of the tissues where they lodge 
to proliferation, and to the production of new tissue morphologically 
identical with tubercle tissue in its various phases (Fig. 92). Coag- 
ulation necrosis, however, does not occur. Dead tubercle bacilli are 
also markedly cbemotactic and capable of causing local suppuration 
and abscess. 1 

1 For further details concerning the effects of dead tubercle bacilli in the body see 
Prudden and Hodenpyl, New York Medical Journal, June 6th and 20th, 1891, and 
Prudden, ibid., December 5th, 1891. 



THE INFECTIOUS DISEASES. 223 

It would seem probable then that while the power of the tubercle 
bacillus to induce necrosis and the fever which in many cases indi- 
cates a systemic intoxication, may be due to metabolic products of 
the living germ, the local lesions characteristic of exudative and pro- 
ductive inflammation may be due to a peculiar bacterio-protein which 
is set free by the disintegration of the bacilli in the tissues. 

The number of bacilli which are present in the lesions of tuber- 
culosis is subject to great variations. They are usually abundant in 
the walls and contents of phthisical cavities, and in tubercle tissue 
which is undergoing cheesy degeneration and disintegration. In 
these situations they may be found in myriads, forming sometimes a 
large part of the disintegrated mass. They are found in cells and 
scattered among them. Sometimes they are present in considerable 
numbers in the giant cells of miliary tubercles. In the acute general 
tuberculosis of children they are often present in large numbers, par- 
ticularly in the lungs (Fig. 91) . They may be found in tuberculous in- 
flammation in any part of the body, and have been seen in the blood. 
The bacilli are almost constantly discharged in the sputa of patients 
suffering from pulmonary tuberculosis, often in enormous numbers — 
from one to four billion in twenty-four hours, according to Nutall's 
estimate — and their presence sometimes affords valuable diagnostic 
aid in early stages of obscure forms of the disease. 

Under a variety of conditions, especially in the older tuberculous 
lesions, the bacilli may not be demonstrable. This apparent occa- 
sional absence of the bacilli is probably due either to their disappear- 
ance as the process grows older, or to some unknown changes which 
interfere with the ordinary staining procedures. 

In human beings cases of direct local inoculation of tuberculosis 
in the skin and accessible mucous membranes have been reported, but 
they are not very common. 

There is no doubt that the bacilli may be introduced into the ali- 
mentary canal by infected milk and meat of tuberculous cattle. 

They may be transmitted from the sick to the well by means of 
the sputum, which is allowed to dry and becomes pulverized and 
which is inhaled as dust, and this, under the ordinary conditions of 
modern life, is the chief means of infection. 

Whether the tubercle bacillus can enter the tissues of the body 
through intact mucous membranes, or whether a lesion, however 
minute, is a necessary condition is not yet fully determined. The 
observations of Loomis and others on the occurrence of tuberculous 
bronchial lymph nodes in persons exhibiting no appreciable tubercu- 
lous lesions elsewhere would indicate the probability of access of the ba- 
cilli to the lymph channels without primary lesion at the portal of entry. 

Tuberculin. — When the tubercle is grown on glycerinated nutri- 



224 THE INFECTIOUS DISEASES. 

ent broth certain metabolic products are formed and pass into solutic 
in the fluids. If after some weeks of vigorous growth the germs a 
separated by filtration and the broth concentrated by evaporation, 
dark-brown fluid results which is called tuberculin. This substan 
— at one time believed by many, and still by a few observers, to pc 
sess distinct curative properties in certain forms of tuberculosis — h 
assumed great economic importance on account of its value as 
diagnostic agent in bovine tuberculosis. For it is found that 
administered subcutaneously in small quantity to cattle, a deflni 
and marked temperature reaction follows in tuberculous anima] 
while those which are sound are unaffected. The existence of ev< 
very slight lesions may be detected in this way. In man also tube 
culin has proved of value in cases in which the efforts to establish 
diagnosis by the usual method have proved futile. 

Concurrent Infection in Tuberculosis. — A concurrent infecti< 
with the tubercle bacillus and other pyogenic micro-organisms is 
extreme significance in that phase of tuberculous inflammation of tl 
lungs commonly called phthisis (see page 459). ' While the so-call( 
cold abscesses may be caused by the tubercle bacillus alone, th 
germ is not infrequently found under these conditions to be associat< 
with other pyogenic micro-organisms, especially the streptococci 
and staph} 7 lococcus. 



METHODS OF STAINING THE TUBERCLE BACILLUS. 

In Fluids. — For the examination of fluids, such as sputum, 2 etc 
the material should be spread in a thin layer on a cover glass, dri( 
in the air, and then passed thrice through the flame (see page 155) 

While, as has been said above, the tubercle bacillus is stain* 
much less easily with the anilin dyes than are most bacteria, it c* 
be deeply colored by the use of accessory agents which intensify t] 
stains or render the protoplasm of the bacilli more accessible to ther 
But when once stained the tubercle bacillus clings with great tenaci 
to its color in the presence of the usual decolorizing agents. 

A variety of methods are in vogue for staining the tuberc 
bacillus, most of them being more or less unessential modificatio: 
of the original process formulated by Koch and Ehrlich. The star 
ing fluid which we have found most generally useful is known ; 
Ziehl's solution. This is made by adding to a five-per-cent aqueoi 

1 Consult Spengler, Zeitschrift f. Hygiene, etc., Bd. xviii, p. 342, 1894 (Biblio 
raphy. 

2 It is well in obtaining sputum for examination in cases of suspected pulmona 
tuberculosis to secure that which has been raised during several hours, including t 
early morning discharge. 



THE INFECTIOUS DISEASES. 225 

solution of carbolic acid about one-tenth its volume of saturated 
alcoholic solution of fuchsin. This carbolic fuchsin will keep un- 
changed for a long time. 

The prepared cover glass is floated in a watch glass or porcelain 
capsule — specimen side down — on this coloring fluid, and gently 
heated almost to boiling for from three to five minutes. 

The entire specimen is thus completely stained, tubercle bacilli, 
tissue elements, and other bacteria which may be present, all in the 
same way. The next step is to remove the color with acid from all 
the structures which may be intermingled with the tubercle bacilli ; the 
later, owing to the tenacity with which they retain the color, being 
but slightly affected. This is done by dipping the cover glass into 
an aqueous or alcoholic solution of five-per-cent sulphuric acid, and 
shaking it about for a few seconds. The acid may be even a little 
more dilute than this. Under the influence of the acid the specimen 
on the cover glass loses its red color and becomes gray or colorless. 
It is then thoroughly rinsed in three or four successive portions of 
alcohol, and finally in water. By this manipulation the red color 
may be to a slight extent restored. 

Care should be taken not to expose the specimen too long to the 
action of the acid, because then the bacilli may be also partially or 
completely decolorized. A little experience will enable the experi- 
menter to judge of the proper time for the action of the acid. 

The specimens may be studied in water with the use of an oil 
immersion and the Abbe condenser, or they may be dried, in the air 
and mounted in balsam. 

Inasmuch as not infrequently some other bacteria besides the 
tubercle bacilli retain a slight red color, it is well, after the specimen 
is rinsed in water, to float the cover glass for a few minutes in a 
dilute aqueous solution of methylen blue, which will replace the red 
color in all of the bacteria except the tubercle bacilli and which 
might be mistaken for it, forming a marked color contrast between 
them. The contrast stain should not be intense. 

Various other anilin dyes may be used instead of the fuchsin, and 
there are various minor modifications of the process which are often 
employed; but, on the whole, for routine sputum examinations we 
recommend the method here given. 

In Sections. — Thin sections of tuberculous tissue which has been 
hardened in alcohol are stained in the same way, except that instead 
of drying and fixation by heat the sections should be fixed to the cover 
glass by means of the albumen fixative (see page 59), and then 
cover glass and section are manipulated together. 

When differentiation is complete the section is cleared in oil of 
cloves or cedar or origanum and mounted in balsam. 
19 



226 THE INFECTIOUS DISEASES. 

For purposes of simple recognition of the bacilli in sections : 
sterns to the writer usually better to have no color in the preparatio 
other than that which the tubercle bacilli possess. But it is ofte 
convenient to demonstrate the nuclei of the cells at the same tim< 
and this may be accomplished by staining lightly afterward with 
dilute solution of some color which will contrast with that of tl 
bacilli, such as Bismark brown or methylen blue. 

In the examination of urine for the presence of the tubercle baci 
lus it is well to collect the sediment by means of a centrifuge 
machine. In the examination of milk, or other fat containing fluic 
for tubercle bacilli, it is well, after the film has been formed upon tr 
cover glass and before staining, to rinse with chloroform followed t 
alcohol, and this by water. 

Occasionally one finds in urine acicular crystalline bodies coi 
siderably resembling the tubercle bacillus in size and shape, an 
retaining a red color after the decolorization of the specimen, 
careful study of the form, however, will suffice to prevent mistakes 

The only other bacilli which are liable to be mistaken for tl 
tubercle bacilli are the bacillus of leprosy and the so-called smegn 
bacillus which sometimes occurs beneath the prepuce. The lepra bac 
lus may be distinguished from the tubercle bacillus by the folio wir 
differential staining process: If the lepra bacillus be stained for t< 
minutes in a dilute alcoholic solution of f uchsin (five drops of saturate 
alcoholic solution of fuchsin to 3 c.c. of water), and then rinsed f« 
a few seconds in a solution of nitric acid (1 part) in alcohol (10 parts 
it will retain a red color, while under the same treatment the tuberc 
bacillus remains uncolored. 

The smegma bacillus is readily decolorized by alcohol after stai: 
ing by Ziehl's solution, and is thus to be distinguished from tl 
tubercle bacillus. 

The bacillus described by Lustgarten as occurring in syphilit 
lesions resembles the tubercle bacillus in form, but after staining wr 
Ziehl's solution is said to be decolorized by sulphuric acid. So litt 
certainty exists, however, as to the existence or significance of tl 
so-called syphilis bacillus that differential staining methods are n 
now to be considered as trustworthy (see page 234) . J 

1 The announcement of the discovery of the Bacillus tuberculosis by Koch w 
made in the Berliner klin. Wochenschrift, 1882, No. 15. A most elaborate and val 
able article on the same subject by Koch is contained in the " Mittheilungen aus de 
Kaiserlichen Gesundheitsamte, " vol. ii. 

The very voluminous literature on the subject of the tubercle bacillus which h 
accumulated since 1882 is for the most part scattered through the German, Englis 
and French journals. It may be best obtained by consulting files of the Ind< 
Medicus of dates since April, 1882, or Banmgarten's " Jahresbericht tiber die Foi 
schritte in der Lehre von den pathogenen Mikroorganismen. " 



LUPUS AND OTHER FORMS OF TUBERCULOSIS OF 

THE SKIN. 

Local tuberculous inflammation of the skin may occur in the form 
of small nodules or wart-like thickenings, as the result of accidental 
inoculation. Local skin infection may occur about the orifices of the 




Fig. 



-Lupus of Face. 



body in tuberculous persons from contact with secretions or excretions 
containing the tubercle bacilli, or about sinuses leading to tuberculous 
abscesses, joints etc., or in the vicinity of tuberculous lymph nodes. 
Finally, a chronic form of tuberculous inflammation which presents 



228 THE INFECTIOUS DISEASES. 

special clinical features has long been known under the name 
lupus. 

Lupus. — This form of inflammation most frequently occurs in t] 
skin of the face, but also in the mucous membrane of the mout 
pharynx, conjunctiva, vulva, and vagina. The lesion consists 
small, multiple nodules of new-formed tissue, somewhat resemblii 
granulation tissue, in the cutis or mucosa and submucosa. By t] 
formation of new nodules and a more diffuse cellular infiltration 
the tissue between them, the lesion tends to spread, and by the confi 
ence of the infiltrated portions a dense and more or less extensive ar< 
of nodular infiltration may be formed. There may be an excessr 
production and exfoliation of epidermis over the infiltrated area, < 
an ulceration of the new tissue. 

Microscopical examination shows the lesion to consist of sm? 
spheroidal cells intermingled with variable numbers of larger, s 
called epitheloid cells and cell masses, and in many cases contaii 
giant cells (Fig. 93). In some cases a well-marked reticulum 
present between the new cells, and these are often grouped in mass 
around the blood vessels. In some cases there is, without previoi 
ulceration, a formation of new connective tissue in the diseased are 
and a well-marked cicatrization; in other cases the cells and inte 
cellular substance undergo a disintegration which leads to ulceratio: 

The morphological characters of the lesion long ago led to tl 
conjecture that lupus was in reality a form of tuberculous inflamm 
tion. This view has now become established by the numerous obse 
vations which show the very constant presence of the tubercle bacilli 
in small numbers at the seat of inflammation. 

In the clinical group of diseases called lupus there are other forn 
of lesion which are not caused by the tubercle bacillus. 



LEPRA (LEPROSY). 

This disease is very common in India and in other hot countries. 
It is not common in America, but in the Gulf States, in Mexico, 
among the Norwegians in the Northwest, and in the eastern British 
provinces a considerable number of cases are grouped. Isolated 
cases are, however, encountered now and then in various parts of the 
United States. 

Leprosy is characterized by the development of nodular and some- 
times diffuse masses of tissue, consisting of larger and smaller cells 
■of various shapes — spheroidal, fusiform, and branched, with a fibrous 
stroma — the whole somewhat resembling granulation tissue. The 



^ ^ ^4i> 




Fig. 94.— The Bacilli of Leprosy. 
Stained with gentian violet. From a nodule in the skin. 

new tissue is most frequently formed in the most exposed parts of the 
skin, as the face, hands, and feet, but it may occur in the skin of any 
part of the body. It is formed more rarely in the subcutaneous con- 
nective tissue, in intrafascicular connective tissue of nerves, in the 
viscera, and in the mucous membranes. The mucous membranes 
most frequently affected are those of the eye, nose, mouth, and larynx. 
The nodules may be very small or as large as a walnut, and may be 
single or joined together in groups or masses. The tissue of the part 
in which the new formation occurs may be atrophied and replaced 
by, or may remain intermingled with, the leprous tissue, or it may 
be hypertrophied. The nodules may persist for a long time without 



230 THE INFECTIOUS DISEASES. 

undergoing any apparent change, or they may soften and breal 
down, forming ulcers; but ulceration, except in the mucous mem 
branes, is said usually to occur as the result of injury or unusua 
exposure. The leprous tissue may change without ulceration int< 
cicatricial tissue, or cicatrization may follow ulceration. 

Various secondary lesions and disturbances of nerve function ar< 
associated with the formation of leprous tissue in the nerve anc 
central nervous system, but these we cannot consider here. 

In all the primary lesions of leprosy, bacilli are said to be present 
mostly in the cells, and particularly in the larger transparent sphe 
roidal forms, but sometimes free in the intercellular substance. Th 
bacilli have been found in the skin, mucous membrane of the moutl 
and larynx, in peripheral nerves, in the cornea, in cartilage, in th 
testicles, and in lymph nodes. Sometimes the cells contain but fe\> 
bacilli, but they are frequently crowded with them. The bacilli ar 
from 4 to 6 a long and very slender, being usually less than 1 v ii 
thickness. They are sometimes pointed at the ends and sometime 
present spheroidal swellings (Fig. 94). In their comportment towar< 
staining agents, as well as in general morphological characters, the; 
considerably resemble the Bacillus tuberculosis, but they are mor 
readily stained. They may be stained with fuchsin or gentian viole 
by the ordinary method, or by the method employed for staining th 
tubercle bacillus (see page 224). 

According to Neisser, the lepra bacillus may be artificially culti 
vated at body temperature on blood serum and on boiled eggs. 

Bordoni-Uffreduzzi claims to have grown it on glycerinated blooi 
serum. It is said by Byron to grow on glycerin -agar with two pe 
cent of sugar, in tubes sealed to retain the moisture. 1 But thes 
reports of success in the artificial cultivation of the lepra bacillu 
have not yet received the seal of experimental confirmation. 

Lepra is communicable from man to man by direct inoculation 
Under modern and proper sanitary conditions the disease is nc 
readily communicable. In a few cases animal inoculations hav 
been made with what appears to be positive results. 

The structure of the new tissue growth, the absence of coagulatioi 
necrosis, and the peculiar grouping of the bacilli in the large trans 
parent cells are characters which usually clearly distinguish th 
lesions caused by the leprosy bacillus from those of tuberculosis. 

1 Byron, New York Pathological Society, January 27th, 1892. 



SYPHILIS. 

The lesions of this form of infectious disease are in many respects 
morphologically similar to those of tuberculosis, and are unquestion- 
ably due to the presence in the body of some form of micro-organism. 




Fig. 95.— Small Nodule of Syphilitic Inflammation (Miliary Gumma) in the Liver. 



I 






%m 






Ik M 






♦ 4 






Fig. 96.— New-formed Tissue in Syphilitic Inflammation. 
From a 'hard chancre, 11 showing swollen endothelium in a small blood vessel. 



232 THE INFECTIOUS DISEASES. 

That this is so, however, we do not know by direct observation and 
experiment, but by inference. 

The characteristic lesions of syphilis consist in a more or less 
circumscribed formation of new tissue. This new tissue may be 
made up largely of small spheroidal cells (Fig. 95), or of these witl 
polyhedral cells and of occasional giant cells. All of these new eel 
masses, which may be very small or occupy large areas, tend tc 




V\ '•■■it .•• "?.•■; 

■ ■■■ y. ■•%$&* 



f J"'^,-: ;Sft3P: Htf l&S,A.i:' -llli 




3:6!j^ 

Fig. 97.— Section from a Primary Syphilitic Nodule of the Mucous Membrane of the Moutb 
Showing collections of cells about the blood vessels in the submucous tissue. 

undergo coagulation necrosis and to disintegrate at the centres 
They may be converted into cicatricial tissue. The new tissues ii 
syphilitic inflammation contain, as a rule, few blood vessels. I 
may form diffusely or in circumscribed masses. The endothelia 
cells of the blood vessels near the inflammatory foci in syphilitic 
inflammation are not infrequently swollen and may proliferat< 
(Figs. 96 and 98, B). The vessels may otherwise undergo extensive 
changes. 



THE INFECTIOUS DISEASES. 233 

In the primary lesion, which is called chancre, there may be 
obliterating endarteritis, a small spheroidal cell infiltration of the 
connective tissue (Fig. 9T), proliferation of connective-tissue cells, 
swelling of the vascular endothelium, and an occasional development 
of giant cells. This new tissue may become fibrous or necrotic and 
may ulcerate. 

Following the primary lesion there may be inflammation of the 












\^ o 



S\ - * 









.»* ** 



A \ 









c--A*-vJ 



» "?,►. : 









Fig. 98.— Section of a Portion of a Syphilitic Condyloma of the Mucors Membrane. 

A, CEdematous papilla ; B. swollen endothelial cells in small blood vessels of a papilla : C, pus 
cells in the submucous connective tissue ; D, pus cells in the epithelium ; E. disintegration of the 
epithelium in the superficial portion of the mucous membrane. 

lymph nodes, of the skin and mucous membranes, of the bones and 
viscera. 

One of the most characteristic phases of the secondary inflamma- 
tions of syphilis results in the formation in the periosteum or the 
viscera of masses of new tissue called gummata. 

The smaller gummata consist of a mass of small spheroidal and 
epithelioid cells (see Fig. 95). As these cell masses grow larger they 



234 THE INFECTIOUS DISEASES. 

are apt to become necrotic at the centre, and we may then have, ai 
seen by the naked eye, a grayish -white, usually firm mass, with i 
more or less dense and irregular cheesy centre and a translucent 
often radially striated border of dense fibrous tissue (see Fig. 247). 

A bacillus closely resembling the tubercle bacillus in form an( 
size has been described by Lustgarten and others as occurring in th< 
lesions of syphilis. It is found in very small numbers. A distinctly 
characteristic mode of staining is not known, and it has never beei 
cultivated on artificial media; so that the evidence that this bacillus 
is the cause of syphilitic inflammation does not appear to us at al 
convincing. 

It is not always easy to distinguish on morphological grounds 
between the lesions of syphilis and those of tuberculosis, but th< 
greater variety in the developmental stages of the tuberculous foe 
which may be found in a single individual; the grouping of th( 
lesions in a manner indicative of progressive local infections, and ir 
the last resort the demonstration of the presence of the tubercl* 
bacillus, will usually suffice to distinguish the tuberculous from th« 
syphilitic lesion, even without recourse to the clinical history. 

For further details regarding syphilitic lesions see Changes in the 
Viscera, Part III. 



GLANDERS. 

Glanders is an infectious disease caused by the presence and 
growth in the body of a bacillus called the Bacillus mallei. 

It is most common in the horse, affecting the mucous membrane 
of the nose (when involving the skin the disease has been called 
farcy), and can be communicated to man and to certain other of the 
domestic animals by direct or accidental inoculations. 

The disease is most frequent in those who come much into direct 
contact with horses. The seat of primary local infection in man is 
most often the skin, more rarely the mucous membranes about the 
nose and mouth. 

The local lesions are similar in man and the lower animals. In 
the presence of the Bacillus mallei there is usually a circumscribed 
or more rarely a diffuse infiltration of the tissue with small spheroidal 
cells — leucocytes — with which new connective- tissue cells (epithelioid 
in form) may be mingled. These whitish foci of cells accumulation 
may be small and to the naked eye resemble miliary tubercles; or, 
they may be larger and nodular. The tissues about them may be 
infiltrated with blood. But the accumulated cells are apt in the 
presence of the bacilli to become necrotic and disintegrate and thus 
lead to smaller and larger abscesses, or, if near the surfaces, to ulcers. 
If occurring on mucous membranes these lesions are often accom- 
panied by intense diffuse catarrhal inflammation. 

As the glanders nodules soften, the bacilli are apt to diminish in 
number or in the capacity to stain, so that it may be possible to 
detect their presence only by inoculation or culture methods. 

The disease may begin at a single point, so that it may be mis- 
taken for a carbuncle or gangrenous erysipelas. But the infection 
is apt not to remain local; the bacilli, finding their way along the 
lymph channels into various parts of the body, set up fresh foci of 
inflammation and necrosis. Then the skin may be covered with a 
pustular eruption; furuncles, carbuncles, and abscesses may form 
beneath the skin and in the muscles. Nodules are found in the nasal 
mucous membrane, the lungs, kidneys, testes, spleen, and liver. The 
joints may be inflamed, and there may be osteomyelitis. 

The glanders infection may, however, pursue a more chronic 
course, with hard, persistent nodules and sluggish ulcers. Under 



236 THE INFECTIOUS DISEASES. 

these conditions the detection of the bacillus in the tissue by a simp! 
morphological examination may be difficult. 

While some forms of glanders nodules somewhat resemble in gros 
and microscopic appearance certain forms of miliary tubercles, tb 
absence in the former of coagulation necrosis and of giant cells, an< 
the tendency to rapid disintegration and softening in the latter wil 
usually suffice for the distinction between the two sets of lesions 
But the demonstration of the bacilli characteristic of each is in al 
cases decisive. 

The Bacillus mallei is a slender bacillus proportionately thicke 
than the tubercle bacillus, with rounded ends, occurring singly or ii 
pairs (Fig. 99). It stains easily with the anilin dyes, but readil; 
gives up the color in presence of even feeble decolorizing agents sue] 
as dilute alcohol or acids. It is left decolorized by Gram's method 
When stained, uncolored areas are apt to remain in the body o 



Fig. 99.— Bacillus Mallei. 

the germ. Whether these are spores or not is not yet definite! 
determined. 

In the tissues the bacilli may be stained with Loffler's alkalin 
methylen blue, or with Ziehl's solution, great care being taken not t 
stain too deeply lest in the decolorization which is to follow the bacil] 
as well as the tissue elements may lose their color. It is well t 
decolorize in very dilute acetic acid (1 : 300), then wash carefully ii 
water, dry the section on the slide with blotting paper and ver; 
gentle heat,' clear with xylol, and mount in balsam. 

T^he glanders bacillus grows readily on almost all of the ordinar 
artificial culture media, and best at blood heat. The growths on soli< 
media are apt to be viscid. On potatoes it forms in two or thre 
days an abundant yellowish pellicle which in a few days darkens an< 
finally becomes brown in color. It gradually loses its virulence ii 
successive generations of artificial cultures. The germ is easil; 
killed by moist heat, but may remain alive in a dried state fo 
months. Field mice and guinea-pigs are very susceptible to infectio] 
with the Bacillus mallei, and after inoculation develop highly char 
acteristic local and general lesions. 

In cases in which an early diagnosis is imperative it is well, ii 



THE INFECTIOUS DISEASES. 237 

addition to the morphological examination and cultures of the sus- 
pected exudate, to inject a small amount into the peritoneal cavity of 
a male guinea-pig. If the virulent glanders bacilli be present, within 
two or three days the testicles will swell and develop an intense sup- 
purative inflammation. 

As the glanders bacillus grows in nutrient broth a proteid sub- 
stance — or substances — develops, which when concentrated by evapo- 
ration of the broth is called mallein. This substance prepared and 
administered to horses suffering from glanders, as tuberculin is pre- 
pared and administered to tuberculous cattle (see page 224), gives a 
similar temperature reaction, and is thus an important diagnostic 
agent, 



EHINOSCLEROMA. 

This disease, which occurs especially in eastern Europe and occa- 
sionally in other parts of the world, is a chronic inflammation of the 
nasal, pharyngeal, and laryngeal mucous membrane. In this inflam- 
mation a diffuse or nodular formation of new tissue, somewhat re- 
sembling granulation tissue, occurs, which tends to assume a dense 
cicatricial character. 

Constantly associated, it is said, with this lesion is a bacillus callec 
Bacillus rhinoscleromatis! This bacillus in most of its morpho- 
logical and biological characters closely resembles the pneumobacillus 
of Friedlander, growing readily on the common culture media anc 
developing a capsule, and it may be identical with it. 

The relationship of this bacillus to the lesions of rhinoscleroma dc 
not appear to be as yet definitely established, since inoculations ir 
men and animals have not given positive results. 



BUBONIC PLAGUE. 

(Oriental Plague; Black Death.) 

This readily communicable arid extremely fatal infectious disease 
is especially characterized morphologically by an acute inflammatory 
swelling of the lymph nodes, most often those of the inguinal region, 
which are apt to suppurate or to become gangrenous. Haemor- 
rhages are common. Carbuncles may occur. 

This disease, formerly not uncommon, has gradually become ex- 
tinct in Europe. In the early summer of 1894 a severe epidemic 
occurred at Hong-Kong, and both Kitasato and Yersin discovered 
that the disease is caused by a short, thick, motile bacillus with 
rounded ends, staining more deeply at the ends than in the middle. 
It grows readily on the ordinary culture media at blood heat, and on 
inoculation into mice, rats, guinea-pigs, and rabbits effects are pro- 
duced similar to those of the disease in man. The bacilli are present 
in the blood, in the lymph nodes, and in the viscera. The germs 
appear to gain entrance to the body through the abraded skin, the 
lungs, and the gastro-intestinal tract. 1 



1 Consult Yersin, Calmette and Borrel, Annales de l'lnstitut Pasteur, July, 1895. 
589. 



TYPHOID FEVER. 

Typhoid fever is an infections disease constantly associated with 
a bacillus called the Bacillus typhi abdominalis. 

The lesions of typhoid fever are usually well marked and con- 
stant. They may conveniently be divided into two classes : 

I. Those lesions which are characteristic of the disease. To this 
class belong the hyperplasia and ulceration of the lymph nodules 
(lymph follicles) of the intestine ; the hyperplasia of the mesenteric 
lymph nodes (lymph glands) , and of the spleen. 

II. Those lesions which frequently occur with this fever and yei 
are not peculiar to it. To this class belong the parenchymatous 
degenerations in the viscera, especially in the liver and kidney; hyalir 
degeneration of voluntary muscles; suppurative inflammation ir 
various parts of the body ; endarteritis and thrombosis, infarctions 
complicating pneumonitis, etc. 

I. The Intestines. — The lesions of the intestines consist of ar 
inflammatory enlargement (hyperplasia) of the solitary lympl 
nodules and of the agminated lymph nodules (Peyer's patches) 
Necrosis of the nodules with ulceration frequently follows the hyper 
plasia. 

The process appears to begin with a catarrhal inflammation of th( 
mucous membrane, accompanied or immediately followed by changes 
in the lymph nodules. The lesions in the lymph nodules begin early 
they have been observed in persons who have died forty-seven hours 
after the commencement of the disease. 

The increase in size of the agminated and solitary nodules maj 
be rapid or gradual. The nodules may be only slightly enlarged, o: 
may project so as to fill up the cavity of the intestine. The enlarge 
ment is usually more marked in the agminated than in the solitary 
nodules. Usually the whole of a Peyer's patch will be enlarged, bu 
sometimes only a part of it. If the enlargement is gradual the dif 
ferent nodules which make up a Peyer's patch are enlarged, whil< 
the septa between them remain but little changed and give the patcl 
an uneven appearance. 

The patches which are only moderately enlarged are of reddish o: 
reddish-gray color, are soft and spongy, and their edges blend grad 
ually with the adjoining mucous membrane. The patches which ar< 



THE INFECTIOUS DISEASES. 341 

more intensely affected are of gray or brownish color, of firm consist- 
ence, and rise abruptly from the surrounding mucous membrane, or 
even overhang it like a mushroom. The largest patches are some- 
times more than three-eighths of an inch thick. 

The enlargement and infiltration may spread from the patches to 
the surrounding mucous membrane, so that the patches appear very 
large ; a number of them may become fused together, and there may 
be even an annular infiltration entirely around the lower end of the 
ileum. 

The infiltration of the Peyer's patches may also extend outward 
into the muscular coat, and even appear beneath and in the peritoneal 
coat as small, gray, rounded nodules. This condition is usually 
found only with a few patches in the lower end of the ileum ; some- 
times in the caecum and appendix vermiformis. These little gray 
nodules usually correspond to diseased patches beneath them ; some- 
times they appear to excite an inflammation of the peritoneum, 
accompanied by the production of numbers of similar nodules all over 
that membrane. Hoffmann describes a case in which the inflamma- 
tion extended to the pleura, with the production of similar nodules 
there. 

The solitary nodules are affected in the same way as Peyer's 
patches. They may be hardly enlarged at all, or be quite prominent, 
or may be affected over a larger portion of the intestine than are the 
patches. Very rarely the solitary nodules are enlarged, while the 
patches are not at all or but slight! j t affected. 

The inflammation and enlargement of the agminated and solitary 
nodules may be followed by a healing process. The character of this 
process varies according to the intensity of the previous inflam- 
mation. 

1. If the disease was mild and the enlargement of the nodules 
moderate, the enlargement gradually disappears and they resume 
their normal appearance (resolution). 

2. In moderate enlargements resolution proceeds first in the 
nodules, leaving the septa between them for a time still swollen and 
prominent. This gives to the surface of a patch a reticulated ap- 
pearance. After a time, however, the entire patch becomes flat- 
tened and uniform. 

3. The solitary nodules or the separate nodules of a patch soften, 
break down, and their contents are discharged with some attendant 
haemorrhage. This leaves a bluish-gray pigmentation, due to altered 
haemoglobin, in the situation of each nodule, and this may remain 
for years. 

4. In more severe types of the disease the enlargement of the 
nodules ends in ulceration. This takes place in two ways: 

20 



242 THE INFECTIOUS DISEASES. 

(a) The enlarged nodules soften, break down, and discharge into 
the intestine. In this way are formed small ulcers. These ulcers 
increase in size by the same softening process, which gradually 
attacks their edges, and in this way ulcers of large size may be 
formed. The ulcers may extend outward only to the peritoneal coat, 
or they may involve the peritoneal coat also and perforate. 

(b) In the severest forms of the disease considerable portions of 
the enlarged patches may slough and become detached, leaving large 
ulcers with thick, overhanging edges. The slough may involve only 
the nodules, or it may involve also the muscular and peritoneal coats. 
These ulcers also may afterward increase in size, and several of them 
may be joined together. 

If the patient recover the ulcers cicatrize, their edges become 
flattened, their floors are converted into connective tissue covered 
with cylindrical epithelium. 

Both forms of ulceration sometimes end in perforation. This is 
effected by the extension of the ulcerative process through the perito- 
neal coat or by the rupture of the floor of the ulcer. Peritonitis and 
death are the usual result. In rare cases, however, the patient 
recovers and the perforation is closed by adhesions. 

The minute changes which take place in the development of the 
intestinal lesion are as follows : 

At first the blood vessels around the nodules are dilated and con- 
gested, while the nodules are swollen and the epithelium falls off. 
Then the nodules increase in size, largely from a growth of new cells. 
The new cells are, in part, similar to the lymphoid cells which nor- 
mally compose the nodules ; in part are large, rounded cells, some of 
which contain several nuclei. The production of new cells is not 
confined to the nodules, but extends also to the adjacent mucous mem- 
brane. In many cases also little foci of the same cells are found in 
the muscular, subserous, and serous coats. This increased number 
of cells compresses the blood vessels and the parts become anaemic. 
Soon the cells, degenerate, either by granular degeneration of indi- 
vidual cells or by gangrene of part of a nodule. In either case 
the degenerated portion is eliminated into the intestine and leaves 
an ulcer of which the floor and edges are infiltrated with cells. 
After this the cell growth goes on and the ulcer enlarges, or the 
cells are gradually replaced by connective tissue and cicatrization 
follows. 

The lesions which we have described are found most frequently 
and are most pronounced in the lower part of the ileum. They are 
not always, however, confined to this situation. Enlarged and ul- 
cerated nodules may be found over the entire length of the ileum and 
even in the jejunum. They may also extend downward and be found 



THE INFECTIOUS DISEASES. 243 

in the colon, even as far down as the rectum. The same changes 
may also take place in the appendix vermiformis. 1 

Besides the regular typhoid lesions of the intestines which have 
Deen described, we occasionally meet with others of a secondary and 
more accidental character. 

Gangrene of the intestinal wall sometimes occurs. It most fre- 
quently involves a portion of the walL corresponding to an ulcer, but 
may also affect other portions where no ulcer exists. The process 
may terminate in perforation or in healing. 

Croupous Inflammation may attack the mucous membrane of 
either the large or small intestine. The mucous membrane between 
the typhoid, ulcers is then more or less covered and infiltrated with 
an exudation of fibrin and pus. 

Peritonitis of a mild type is a frequent accompaniment of the 
intestinal lesions. It appears to have but little influence on the 
course of the disease. 

Severe peritonitis is usually due to perforation, less frequently to 
ulcers which reach the serous coat but do not perforate. When there 
is infiltration of the serous coat with the typhoid new growth, the 
peritonitis may be accompanied by a production of little gray nodules 
of the same character throughout the peritoneum. 

Infarctions of the spleen, inflammation of the ovaries, and per- 
foration of the gall bladder are sometimes the cause of peritonitis. 

Haemorrhage from the intestines may be slight and due to the 
inflammatory swelling and congestion of the mucous membrane ; or 
it may be due to the ulceration of the follicles and opening of the 
Hood vessels, and is then often profuse. 

Mesenteric Lymph Nodes. — The mesenteric nodes undergo 
changes similar to those in the nodules of the intestines, and are 
usually affected in a degree corresponding to the intensity of the 
intestinal lesion. 

The nodes are at first congested and succulent ; then there is a pro- 
duction of lymphoid cells and large cells (Fig. 262), as in the intes- 
tinal nodules, and the node becomes enlarged. When the enlarge- 
ment has reached its full size the congestion diminishes and the cells 
begin to degenerate. The degeneration may take place slowly, and 
then the node gradually returns to its normal condition; or more 
rapidly, and then little foci of softened, purulent matter are formed. 
If the patient recovers the small foci are absorbed, leaving a fibrous 

1 Owing to the frequent involvement of Pever's patches the larger intestinal ulcers 
in typhoid fever are apt to have their longest diameter lengthwise of the gut in 
contrast to spreading tubercular ulcers, which, owing to the extension of the local in- 
flammation along the encircling lymph channels, are apt to have the longest diameter 
crossing the gut. But exceptions to this general rule are common. 



244 THE INFECTIOUS DISEASES. 

cicatrix; the larger foci may become dry, necrotic, and enclosed 
a fibrous capsule. The inflammation of the nodes may produce 
local or general peritonitis. Intense exudative inflammation m 
occur in the nodes, which may be densely infiltrated with serui 
fibrin, and pus. 

The Spleen. — In nearly every case of typhoid fever the spleen 
enlarged. This enlargement begins, as a rule, soon after the coi 
mencement of the disease, increases rapidly until the third wee 
remains stationary for a few days, and then diminishes. The org; 
is congested, of dark-red color, and of firm consistence while it 
increasing in size. After it has reached its maximum size its cc 
sistence becomes soft and there is a considerable deposit of bro\ 
pigment. The enlargement appears to be due to congestion a; 
hyperplasia (compare page 624). 

In rare cases the softened spleen ruptures, with an extravasati 
of blood into the peritoneal cavity. 

There may be infarctions of the spleen, which sometimes soft 
and cause peritonitis. 

II. The second class of lesions comprises those which are fi 
quently found with typhoid fever, but are not peculiar to it. 

The Mouth. — A number of changes are found about this regio 
The follicles at the root of the tongue and the tonsils may be enlarge 
the muscles of the tongue may undergo waxy and granular dege 
eration; gangrenous ulcers may attack the floor and sides of t] 
mouth and destroy large areas of tissue. 

The Pharynx may be the seat of catarrhal or croupous inflamm 
tion, producing superficial and deep ulcers. 

The Parotid is, in a moderate number of cases, the seat of ; 
inflammation which tends to suppuration. In this process both t] 
glandular acini and the connective tissue between them are involve 
Which of the two has the larger share in the process is still in di 
pute. 

A slight enlargement and induration of the parotid and subma 
illary glands is said by Hoffmann to be a frequent lesion, and 
depend on increase of the gland cells and dilatation of the acini wi 
their secretion. 

The Pancreas undergoes changes similar to those in the saliva: 
glands. It becomes at first swollen and red, then hard and grayis 
then yellow. The vessels are at first congested, afterward there 
increase of the gland cells, and lastly degeneration. 

The Liver may preserve its normal character or may prese: 
changes. 

In many cases the organ will be found swollen, pale, soft ai 
flabby. Minute examination then shows that the liver cells ha^ 



THE INFECTIOUS DISEASES. 245 

undergone parenchymatous degeneration. They are filled with fine 
granules and small fat globules, and the degeneration may go on so 
far that the outlines of the hepatic cells are lost and nothing but a 
mass of granules can be seen. 

Less frequently we find in the liver very small, soft, grayish 
nodules. They are situated along the course of the small veins, and 
there is a,t the same time a diffuse infiltration of lymphoid cells along 
the small veins. The nodules consist of lymphoid cells; they are 
often too small to be distinguished with the naked eye. 1 Small 
necrotic foci are sometimes present. 

The Heart. — In a considerable number of cases the muscular 
tissue of the heart is altered by granular, fatty, or hyalin degenera- 
tion or by pigmentation. Myocarditis, endocarditis, and pericar- 
ditis are of occasional occurrence. 

Thrombi in the cavities of the heart and vegetations on the valves 
are sometimes found. Detached fragments of these may be lodged as 
emboli in the different arteries. 

The Arteries. — There may be an acute inflammation of the ar- 
teries, especially at the commencement of convalescence. There are 
two varieties: an obliterating and a parietal arteritis. In the oblit- 
erating arteritis there is infiltration of all the coats of the artery, 
with roughening of the intima and the formation of a thrombus 
within the vessel, and this may be followed by dry gangrene of the 
part supplied by the artery. In the parietal variety the wall of the 
artery is infiltrated with cells, but the intima is not roughened and 
no thrombus is formed. 

The Veins. — Thrombosis of the larger veins, especially of the 
femoral vein in the third and fourth weeks of the disease, is not un- 
common. 

The Larynx is very frequently the seat of catarrhal inflammation, 
'with or without superficial erosions. Less frequently there is croup- 
ous inflammation, followed in some cases by destructive ulceration. 

The Lungs. — Catarrhal inflammation of the large bronchi is very 
common. Broncho-pneumonia occurs in two forms. There may be 
a severe inflammation of most of the bronchi of both lungs, with 
cellular infiltration of the walls of the bronchi and zones of peribron- 
chitic pneumonia; or there is an intense general bronchitis, with 
lobules of the lung corresponding to obstructed bronchi, either col- 
lapsed or inflamed, or both. 

From the long-continued recumbent position of the patients the 
posterior portions of the lungs become congested, dense, and un- 

1 Reed, " An Inveatigation into the so-called Lymphoid Nodules in the Liver in 
Typhoid Fever, " American Journal of Medical Sciences, November, 1895. Johns 
Hopkins Hospital Report, vol. v., p. 379. 



246 THE INFECTIOUS DISEASES. 

aerated. Sometimes, in addition to this, irregular portions of the 
lungs become hepatized. Less frequently there is a regular acute 
lobar pneumonia. There may be infarctions. 

Gangrene of the lungs occasionally occurs, either associated with 
lobular pneumonia or with infarctions, or as an independent condition. 

Fibrinous pleurisy and empyema occasionally occur. 

The Kidneys very frequently present the lesions of acute degen- 
eration, and occasionally those of acute inflammation. Small collec- 
tions of lymphoid cells and small abscesses may be found in the 
kidney. 

Catarrhal and croupous inflammation of the bladder may occur. 

The Ovaries. — Hsemorrhage and gangrenous inflammation have 
been observed in rare cases. 

The Testicles. — Orchitis has been described. 1 It is usually de- 
veloped during convalescence ; is unilateral ; and usually affects the 
testicle alone, less frequently the epididymis; it may terminate ir 
suppuration. 

The Brain. — Acute meningitis is rare. Thrombosis of the 
venous sinuses, and obliterating endarteritis of the cerebral arteries, 
are occasionally observed. 

The Voluntary Muscles, especially the abdominal muscles, the 
adductors of the thigh, the pectoral muscles, the muscles of the dia- 
phragm and of the tongue, frequently undergo the hyalin degenera- 
tive changes described under muscle lesions. 

The Skin. — Gangrenous inflammation of the skin frequently 
occurs in the form of bed sores, affecting especially the skin over the 
sacrum and trochanters, where it is subjected to the constant pres- 
sure of the bed. 

There may be suppurative inflammation in almost any part of the 
body. Perhaps the most important of these local suppurations is 
that which results in retropharyngeal abscess. 

The post-typhoid bone lesions are important. 2 In the secondary 
bone lesions . after typhoid as well as elsewhere the bacillus may 
remain alive for long periods, even several months. 

THE BACILLUS OF TYPHOID FEVER. 

The presence of a bacillus in various parts of the body in typhoid 
fever, in a considerable proportion of the cases examined, has been 
well established by a large number of observers. This bacillus does 
not occur in the body, so far as is known, except in connection with 
this disease. 

1 Ollivier, Rev. de Med., November and December, 1883. 

2 Parsons, Johns Hopkins Hospital Reports, vol. v., p. 417. 



THE INFECTIOUS DISEASES. 247 

In the early stages of the disease the bacillus may be found in the 
lymphatic structures of the intestines and in the mesenteric lymph 
nodes and the spleen. It may be present in the bone marrow, kidney, 
liver, bile, lungs, and in the blood, and it may be found, though not 
in such abundance as was formerly assumed, in the intestinal con- 
tents after the disease had become well established. In the viscera 
it is apt to occur in larger and smaller masses or clusters (see Fig. 
100). It has been repeatedly found in the urine. The typhoid bacilli 
may be present alone or in association with other germs in the foci of 
suppuration which so frequently complicate typhoid fever, also in the 
exudates in inflammations of the serous membranes and in the endo- 
cardial vegetations. 1 

The typhoid bacillus is usually about three times as long as broad, 
being about one-third as long as the diameter of a red blood cell. 




Fig. 100.— Cluster op Typhoid Bacilli in the Spleen. 

But it varies considerably in size when growing on different media. 
It is rounded at the ends, and frequently contains rounded structures 
which have been regarded as spores, but which further researches 
have led us to believe are not spores but vacuoles. The bacillus is 
beset with flagella. 

The typhoid bacillus can be readily cultivated on the ordinary 
culture media at room temperature. It forms delicate, bluish-white, 
sinuous-edged, spreading colonies on the surface of nutrient gelatin, 
which it does not fluidify. Several other bacteria grow in a similar 
way on gelatin. The growth of the typhoid bacillus on boiled potatoes, 

1 See Flexner, Journal of Pathology and Bacteriology, April, 1895, and Johns 
Hopkins Hospital Reports, vol. v., p. 343. Also for full consideration of the pyo- 
genic powers of the typhoid bacillus consult DmocJiowsM and Janowski, Ziegler's 
Beitr. z. path. Anat., etc., Bd. xvii., p. 221. 



248 THE INFECTIOUS DISEASES. 

in a nearly invisible pellicle, is a marked culture characteristic. If, 
however, the potato be slightly alkaline the surface growth becomes 
evident. In cultures the typhoid bacilli often cling together end to 
end, forming long, thread-like structures (Fig. 101). The bacilli in 
fluids are actively motile. 1 

Inoculations of the tynhoid bacillus into animals, while not pro- 
ducing a disease in all respects like that in the human subject, may 
cause death with symptoms and lesions as closely resembling those 
in man as we are often able to produce in animal experimentation. 
Although similar effects may be induced in animals by the inocula- 
tion with other germs, the evidence that typhoid fever in man is 
produced by the typhoid bacillus, and by this alone, is altogether so 
strong as practically to amount to a demonstration. 

It is probable that the usual symptoms and lesions of typhoid 
fever are largely due to the absorption of toxic substances which are 
produced as the result of the life processes of the bacteria at the point 
of their greatest accumulation and activity. 



Fig. 101.— Bacillus Typhosus. 
From a gelatin culture. 

During artificial cultures in nutrient broth a poisonous albuminoid 
product or products are formed and have been named typhotoxin. 
Injection into rabbit may in addition to general toxic symptoms 
induce hyperplasia of the intestinal lymph nodes. 

Some of the inflammatory complications which occur in typhoid 
fever are due to the growth of the bacillus in unusual places in the 
body, but many of them are due to a secondary infection with other 
germs, notably with the pyogenic cocci. 

Infection with the typhoid bacillus seems to occur largely through 
the gastro-intestinal canal. 

In a large proportion of cases the disease is communicated by 
means of food, and especially of milk and drinking-water which have 
been polluted with the excretions of persons suffering from the 
disease. Many serious epidemics of typhoid fever have been traced 

1 Several bacilli are known which considerably resemble the typhoid bacillus in 
form and general biological characters under cultivation. Most noteworthy among 
these is the Bacillus coli communis, which is a constant resident of the gastro- 
intestinal canal. This germ, which in the past has no doubt been frequently mis- 
taken for the Bacillus typhosus, may now be differentiated from it. 



THE INFECTIOUS DISEASES. 249 

to pollutions of milk and drinking-water from such sources. 1 Oysters 
which have been taken from grossly polluted waters, as near sewer 
openings, have been the means of conveying the germs. 2 

In milk the typhoid bacillus not only remains alive for long 
periods but undergoes active multiplication. It may remain long 
alive in water and even for a time multiply. In the soil and when 
dried it may remain alive for months. Frozen in ice it has been 
found alive after more than three months. It is readily killed by 
exposure to strong sunlight. 



METHODS OP STAINING THE TYPHOID BACILLUS. 

The bacilli, when taken from cultures, stain readily with the 
ordinary anilin dyes, such as fuchsin and gentian violet (see page 
130.) 

In sections of the organs they do not take the stain so readily. 
They are decolorized by Gram's method. 

One of the most satisfactory solutions for this purpose is that of 
JZiehl, which is made as follows: 

Filtered saturated aqueous solution of Carbolic Acid, 90 
Saturated alcoholic solution of Fuchsin 10 

The sections are soaked for half an hour in this solution and then 
•decolorized by alcohol, cleared in oil of cedar, and mounted in balsam. 
The decolorization should be done carefully, the section being ex- 
amined from time to time as it proceeds, so as to avoid the removal 
of too much color. The nuclei should remain faintly colored, but 
not so much so as to conceal the clusters of more deeply stained 
bacilli. 3 

1 Freeman, New York Medical Record, March 28th, 1896. 

2 Foote, Medical News, March 23d, 1895. 

3 For recent summary of studies on the typhoid bacillus and typhoid fever, with 
bibliography, consult Dunbar, "Ergebnisse der allg. Aetiologie der Menschen- u. 
Thierkrankheiten, " 1896, p. 605. 



DIPHTHERIA. 

Diphtheria is an acute infectious disease caused by the Bacilh 
diphtheriCE (Loftier), and usually characterized by a pseudo-men 
branous inflammation on some of the mucous membranes or oca 
sionally on the surface of wounds, and by immediate or remote effec 
of absorbed toxic substances. 

The mucous membranes which are the most frequently affecte 
in diphtheria are those of the tonsils, pharynx, soft palate, nare 
larynx, and trachea ; less frequently those of the mouth, gums, coi 
junctiva, oesophagus, and stomach. 

The local inflammation in mucous membranes may present varioi 
phases, which represent clinical types of the disease. Thus the: 
may be a simple redness of the affected surfaces which leaves no tra< 
after death, or a catarrhal inflammation. On the other hand, in tl 
more marked forms of the lesion there may be a fibrinous exuda 
which infiltrates the mucous membrane, or, intermingled with pi 
cells, epithelial cells, red blood cells, bacteria, and granular materia 
forms a thick or thin pellicle on the affected surfaces. This pellic 
may undergo coagulation necrosis, and hand-in-hand with this the: 
may be superficial or deep coagulation necrosis of the mucous men 
brane. 

The false membrane in diphtheria is thus formed by a combinatic 
of inflammation and necrosis, the extent of the necrosis and tl 
amount of inflammatory products varying in the different cases. 

The pseudo-membrane may disintegrate or exfoliate, with < 
without loss of tissue in the underlying mucous membrane. Phle^ 
mon, abscess, and oedema are liable to occur as local complication; 
Adjacent and distant lymph nodes are apt to be swollen, and ofte 
show, on microscopical examination, small foci of cell necrosis an 
disintegration. Similar necrotic foci and areas of small spheroida 
cell accumulation with fatty degeneration may be found in tr. 
kidney, spleen, and liver. Acute nephritis and degeneration of tr. 
heart muscle are not infrequent. 1 The exact nature of the nerv 
lesions which may be associated with the late paralyses of diphtheri 
is not yet clear. 

1 For a study of heart lesions in diphtheria consult SehamscMn, Ziegler's Beitr. : 
path. Anat., Bd. xviii., p. 64, 1895. 



THE INFECTIOUS DISEASES. 251 

Catarrhal bronchitis and broncho-pneumonia or lobular pneumonia 
frequently complicate diphtheritic lesions of the upper air passages 
and fauces. 

Bacteria of various forms are commonly present in the false 
membrane, and some of the forms may penetrate deeply into the 
underlying tissue. The germ, however, which stands in a causative 
relationship to this disease is the Bacillus diphtherias of Loffler. 

In man the diphtheria bacilli are largely confined to the seat of 
local lesion, and sometimes occur in enormous numbers (see Fig. 102), 
especially in the older layers of the pseudo-membrane. But they may 
become widely distributed through the blood. The systemic effects 
in diphtheria appear to be due to the absorption into the body of toxic 
material elaborated by the germs. 

The very frequent association of the pyogenic cocci with the diph- 



■^^^t-^^mt 



-v^-. 



: fy : ^ * ;*v>'-;*. ■■/■ :&$m 



-";L-:.-V'-,: : ■ 6 %^.^':~ 



Fig. 102.— Diphtheritic Inflammation op the Tonsil. 
Showing Loffler's bacilli in the pseudo-membrane. 

theria bacillus give rise to a complicating series of results which 
make the clinical picture and the lesions of diphtheria sometimes 
very complex. Thus the complicating bronchitis and broncho-pneu- 
monia, as well as pysemic symptoms and lesions, may be due to the 
presence in the pseudo-membrane, and the entrance into the deeper 
air passages and the blood, of the Streptococcus pyogenes and the 
Staphylococcus pyogenes, the Diplococcus lanceolatus, Bacillus coli 
communis, and others. 

The Bacillus diphtherias, first described and definitely associated 
with this disease by Loffler, is from 2.5 to 3 /j- in length and 0.5 to 0.8. 
P- in thickness, and is characterized morphologically by marked irreg- 
ularities in its form (Fig. 103). While the typical form is that of a. 



252 THE INFECTIOUS DISEASES. 

moderately stout, round-ended, straight, or slightly curved bacillus, i 
is very apt — perhaps as a result of degeneration — to appear club 
shaped or pointed at the ends, irregularly segmented, and to develo 
at the ends or elsewhere a strongly refractile material which stain 
more deeply than the rest of the protoplasm. 

The diphtheria bacillus is immotile, grows slowly and scantily a 
room temperature, but at body temperature develops rapidly in bouil 
Ion and on agar, glycerin-agar, and blood serum. On glucose-brotl 
serum (Loffler's blood-serum mixture) the growth is particularly 
vigorous (see page 162). On glycerin-agar plates it grows in the forn 
of moderately small, grayish white, slightly spreading, rough-edge< 
colonies. According to Welch and Abbott, it grows abundantly in ai 
invisible pellicle on potatoes. It does not form spores. Welch an< 
Abbott have found that in fluids it may be killed by an exposure o 
ten minutes to a temperature of 58° C. But it may remain alive fo 
weeks, or even months, in fragments of dried membrane. 1 




Fig. 103. — Bacillus Diphtherial. 
From exudate in the throat of a case of diphtheria; showing irregularities of the bacilli i 
shape and size and coloration. 

It may be stained with Loffler's alkalin methylen-blue solution o: 
by Gram's method. 

The diphtheria bacillus is subject to extreme variations in viru 
lence, forms being met with in which all the usual cultural character 
istics are not in the slightest degree virulent. These are sometime; 
inadvisably called pseudo-diphtheria bacilli. 

The name pseudo-diphtheria bacillus is more wisely limited t< 
such germs as, though resembling the diphtheria bacillus, still presen 
distinct cultural peculiarities. 1 

Inoculations of virulent cultures subcutaneously in guinea-pig! 
are regularly followed by a localized haemorrhagic oedema with i 
variable amount of whitish exudate. Death usually follows tin 
inoculation in from two to five days. In addition to the local lesion 
there may be — but this is not constant — swelling of the adjacent anc 

1 Consult Park and Beebe, " Report on Bacteriological Investigations ; Diagnosi 
of Diphtheria, " Bulletin No. 1, Health Dept., New York City, 1895; Studies am 
Bibliography. 



THE INFECTIOUS DISEASES. 253 

of the abdominal lymph nodes, serous effusions into the pericardial, 
pleural, and peritoneal sacs, swollen spleen, and acute parenchy- 
matous and fatty degeneration in the liver, kidne} T , and heart muscles ; 
congestion and sometimes haemorrhage of the suprarenals. Micro- 
scopical examination shows, in a considerable proportion of cases,, 
fragmentation of nuclei and other eA r idences of cell death at the seat 
of inoculation and in the viscera. 1 Animals which survive the 
inoculations may later develop paralysis, and a similar result may 
follow the injection into rabbits of culture fluids. The bacilli do 
not gain access to the body at large, but may be found at the seat of 
inoculations. Inoculation into the mucous membranes of rabbits, 
pigeons, and certain other animals may result in the development of 
a pseudo-membrane somewhat resembling that of the disease in 
man. 2 

During the growth of the diphtheria bacillus in nutrient broth an 
albuminous toxic substance is developed which mingles with the 
broth. This is called diphtheria toxin, and subcutaneous injections 
of this toxin in animals — guinea-pigs, for example — proves fatal, in 
appropriate dosage, with symptoms and lesions similar to those caused 
by inoculation with the living germ. 

It has been found that by repeated injections of the diphtheria 
toxins in susceptible animals, at first with small, then with gradually 
increasing doses, the animal may at length become so insusceptible to 
the action of the poison that many times the usually fatal dose is 
borne without sensible reaction. 

Similar immunity can be conferred in certain animals by the use 
of the living cultures of the diphtheria bacillus either fully virulent 
or with reduced virulence (see page 179), administered at first in small 
doses which are gradually increased. 

In whichever way immunity be conferred it has been found that 
the blood of the artificially immunized animal contains a substance, 
or substances, called diphtheria antitoxin, which on being intro- 
duced with the blood serum into other susceptible organisms, may 
not only confer a quickly established immunity, but, without destroy- 
ing the diphtheria germ, may protect against its toxic effects when 
the disease is already under way. Thus through the artificial im- 
munization of horses the so-called " serum therapy "has assumed a 

1 For a detailed description of minute cell changes in animals following inocula- 
tion with diphtheria bacilli, see Welch and Flexner, Bulletin of the Johns Hopkins 
Hospital, August, 1891; also Abbott and Ghriskey, ibid., April, 1893. 

2 It is important from the prophylactic standpoint to remember that the Bacillus 
diphtherias may remain alive in the mouth of the human subject for many weeks 
after recovery from the local lesions of the disease, and also that healthy persons 
when the disease is prevalent may harbor the bacilli in their mouths. 



254 THE INFECTIOUS DISEASES. 

very important and beneficent role in the prevention and management 
of diphtheria. 

Although there is no differential stain for the diphtheria bacillus, 
its morphological peculiarities are, as above indicated, so marked that 
when occurring in considerable numbers in the membranes or when 
examined from serum cultures definite conclusions as to its identity 
can usually be arrived at without recourse to complete biological 
a^atysis. But this as well as animal inoculations will often be 
necessary when the morphological characters are doubtful, and when 
the degree of virulence is to be determined. 

For the practical ends of early diagnosis it has been found that if 
a smear of material from the local lesion be made over the surface of 
a " slant tube" of Loffler's blood-serum mixture, and placed in an in- 
cubator at blood heat for twelve hours, the diphtheria bacilli, if present, 
will usually have outstripped in growth most of the other germs 
which were present in the exudate. If now cover-glass preparations 
be made of a considerable quantity of the new growth which is dotted 
in scarcely visible colonies over the surface of the serum, the presence 
or absence of the diphtheria bacillus can, in a large proportion of 
cases, be determined from its peculiar morphological features (Fig. 
103). This method, elaborated by Park 1 and put into practice on a 
large scale by the Health Department of New York, has now become 
an almost indispensable factor in the control of diphtheria by health 
officials in many parts of the world, and is of especial importance in 
connection with the use of diphtheria antitoxin serum, whose highest 
promise lies in early administration. 

1 Consult Biggs, Park and Beebe, "Report on Bacteriological Investigation and 
Diagnosis of Diphtheria, " Bulletin No. 1, Health Dept., City of New York, 1895. 



TETANUS. 

{Lockjaw. ) 

This disease is caused by a bacillus — Bacillis tetani — which is 
rather widespread and in some places very abundant, occurring with 
other germs in the soil, especially in manured soil, and gaining 
entrance to the body through wounds, which are often very slight. 
The Bacillus tetani is a rather long, slender, motile germ, often 
growing in pairs or threads and prone to develop a spore in one end 
(Fig. 104), under which condition the bacillus swells at the end and 
becomes club or racket-shaped. It is readily stained. At the room 
temperature it grows on artificial culture media, and is strictly 
anaerobic, flourishing in an atmosphere of hydrogen. It fluidifies gela- 
tin after sending out into it irregular-shaped, ray-like outgrowths. 



%k 



Fig. 104.— Bacillus Tetani. 
From a culture. 



The spores of the tetanus bacillus are very resistant to drying, to 
heat, and to various chemical disinfectants. 

Characteristic tetanic symptoms followed by death may be induced 
in mice, guinea-pigs, and rabbits by subcutaneous inoculation of 
cultures. 

Man and the horse are markedly susceptible to tetanus; birds are 
as a rule insusceptible. 

The local lesion in tetanus is usually slight and not characteristic, 
often consisting in a slight suppuration. 

The morphology of the lesions of the nervous system to the exis- 
tence of which the symptoms of tetanus so directly point is yet 
obscure. Overfilling of the blood vessels, cellular exudate into the 
perivascular spaces, and rather indefinite changes in the ganglion 
cells have been recorded. The bacillus remains at the seat of local 



256 THE INFECTIOUS DISEASES. 

lesion and produces its effect by the elaboration of a most inter 
poison or toxin, called tetano-toxin. The action of this toxic si 
stance appears sometimes to continue in the bod} 7 after the death 
the organisms which have elaborated it. This infectious dise£ 
affords a most typical example of toxaemia. 

If the tetanus bacillus be grown in nutrient broth at blood h< 
out of contact with oxygen the toxin is developed and mingles wi 
the fluid. This toxin when freed from living germs is capable 
producing all the symptoms of the disease. 

Broth cultures may after some weeks have acquired such an e 
treme intensity that the dried poisonous material, separated from t 
inert iiuids and partially purified, may be fatal to a mouse weighi 
15 gm. in a dose of 0.00000005 gm. 

Estimating according to the relative weights of the subjects, t 
minimal fatal human dose would be about 0.23 mgm. 

This toxin is rendered inert by a temperature above 65° C. a 
by light. 

By procedures similar to those described in diphtheria immunn 
tion (page 253), the tetanus toxin has been used to secure artific 
immunity in dogs, goats, and horses, and here also the blood sen 
of the immunized animals has been prepared in a dried state a 
employed in man for therapeutic purposes with some degree of si 
cess. 

The theoretical promise of the tetanus antitoxin for therapeu 
purposes in man is, however, in practice rendered in large mease 
futile, because the existence of the disease is not recognizable un 
the toxaemia is sufficiently marked to produce the nervous sympton 
at which time an enormous and not easil} T determined dosage 
required to neutralize or counteract the effects of the already elal 
rated poison. 

Statistics are as yet too meagre to justify a definite opinion as 
the practical value of serum therapy in tetanus. 

For purposes of diagnosis it may be necessary to inoculate a wh 
mouse at the base of the tail with suspicious material at the sai 
time that morphological examination and anaerobic cultures a: 
made. Should tetanus develop in the mouse within a few days cc 
trol cultures may be made from the exudate at the seat of inocu. 
tion. 



INFLUENZA. 

{Epidemic Catarrhal Fever; La Grippe.) 

This is an infectious disease characterized by fever, physical and 
mental prostration, and inflammations of different parts of the body. 
It differs from the other infectious diseases in that, instead of a single 
characteristic lesion, there is a disposition to acute exudative inflam- 
mation of either the pia mater, the sheaths of the peripheral nerves, 
the conjunctiva, the ears, the nose and throat, the larynx, the bron- 
chi, the lungs, the pleura, the stomach, or the colon. Either one or 
several of these inflammations may be developed at the same time, or 
successively in one individual. It is, however, not uncommon to see 
cases of influenza in which no one of these inflammations is present. 

The numerous bacterial studies which up to 1892 had been made 
on epidemic influenza had failed to reveal any micro-organism which 
could fairly be regarded as of etiological significance, although some 
of the complicating inflammations of the lungs had been shown to 
be very frequently associated with the pyogenic cocci — Staphylo- 
coccus pyogenes and Streptococcus pyogenes and the Diplococcus 
pneumoniae. 1 

Early in 1892 Pfeiffer, Kitasato, and Canon 2 described the occur- 
rence in the bronchial exudate and in the blood of influenza patients 
of a very small bacillus, hitherto unknown or possibly noted earlier 
by Babes. This bacillus was sometimes present in the bronchial 
exudate in enormous numbers, and often with little contamination 
with other germs. In the blood it was sometimes abundant, some- 
times scanty. It stains with some difficulty with the simple anilin 
dyes; but by Ziehl's solution (page 224); or hj warmed Loffler's 
methyl blue (page 158) ; or by Czenzysnki's fluid (page 283), heated 
with the specimen at body temperature for from three to six hours, 
it is readily colored. The bacilli are very slender and short (one to 
one and a half times as long as broad), sometimes lie singly, some- 
times in pairs or short chains or heaps, and are not motile. 

This so-called influenza bacillus grows best at body temperature. 
On glycerin-agar it forms very small, scarcely visible dewdrop-like 

1 Consult Finkler, "Die acuten Lungenentziindungen, " 1891, p. 452. 

2 Deutsche medicinische Wochenschrift, January 14th and May 26th, 1892. 

21 



258 THE INFECTIOUS DISEASES. 

colonies; these, although growing close together, do not tend to cos 
lesce, as many germs do. 

According to Pfeiffer the growth is more voluminous if the sui 
face of the agar be smeared with blood — best of man or the pigeon- 
since the haemoglobin appears to favor the growth. It does not gro^ 
at a temperature at which nutrient gelatin remains solid. In bee 
tea it forms a scanty, cloudy growth. It has been cultivated throug 
several generations, but is prone to die. Animal inoculations hav 
given diverse and not very marked results. 

The earlier observations have been in general confirmed by late 
studies of others. 1 

On the whole, we can only say at present that while the occui 
rence of the above-described bacillus in influenza, and exclusive! 
here, is interesting and apparently significant, we cannot yet definite]; 
regard it as of established importance in the etiology of the disease 
The observations of the writer upon this germ have been too limite 
to permit of an independent opinion. 

1 For bibliography and later data consult Beck, "Ergebnisse der allg. Aetiologi 
der Menschen- u. Tnierkrankheiten, " 1896, p. 742. 



BACTERIA WHICH MAY BE OCCASIONAL INCITERS OF 
INFECTIOUS DISEASE IN MAN. 

Bacillus ceclematis maligni. — This bacillus, which is frequently 
present in dust, in putrefying substances, and in garden earth, con- 
siderably resembles the anthrax bacillus in form, but is more slender 
and has rounded ends. When it develops spores the bacillus is 
swollen or bellied at the middle. It is strictly anaerobic, growing 
readily in gelatin-agar and blood serum. It fluidifies gelatin. Gas 
is developed in its growth on blood serum. 

Several times this bacillus has been found in persons who have 
received dirty wounds, and it has been associated with hsemorrhagic 
oedema, gas formation in the tissue, and gangrene. Similar lesions 
are produced by inoculation of the pure cultures in animals. 

This bacillus is readily stained by any of the common anilin 
d3 T es. ] 

Bacillus pneumoniae (Friedldnder) . — In a small proportion of 
cases of lobar and lobular pneumonia, and in a few cases of exuda- 
tive inflammation of the pleura, pericardium, meninges, and middle 
ear, this bacillus has been found. It is sometimes found alone, but 
in pneumonia is frequently associated either with the Diplococcus 
pneumoniae or with the pyogenic cocci. It has been found in the 
nasal secretion and mouths of health} 7 persons. While belonging 
definitely among the bacilli, it so frequently occurs in the form of 
very short rods or ovals or short chains that it was formerly thought 
to belong among the cocci. The bacilli, whether longer or shorter, 
single or in short chains, in cultures as well as in exudates, are sur- 
rounded by a narrow hyalin capsule. 

It grows readily, at ordinary room temperature, in gelatin, which 
it does not fluidify, forming a white mass, which, heaping itself upon 
the surface and less markedly along the puncture line, forms a rather 
characteristic "nail-like" growth. It grows abundantly on other 
culture media. It is moderately pathogenic for mice. It seems 
highly probable rather than proven that it may be at least partially 
responsible for the lesions with which it is infrequently associated 
in man. This germ was formerly believed to be of great importance 

1 Consult Novy, Zeitschrift f. Hygiene, etc., Bd. xvii., p. 209 (bibliography). 



260 THE INFECTIOUS DISEASES. 

in connection with acute lobar pneumonia, and for a time was genei 
ally spoken of as the pneumocccus of Friedlander. It is now know] 
not to be a coccus, and is certainly of subordinate if at all of seriou 
importance in the induction of inflammation of the lungs. 

Its identity with the so-called Bacillus rhinoscleromatis (page 23$ 
is claimed by some observers. If it be not identical with them it i 
closely related to capsulated bacilli found by ISTicolaier * in pus, b; 
Abel 2 in ozcena and found under various conditions and describe^ 
under various names by Bordoni-Uffreduzzi, Pfeiffer, Mori, an 
others. 

Bacillus coli communis ("colon bacillus"). — This germ, whio 
is of constant occurrence in the intestinal canal of man, is commonl; 
reckoned among the saprophytes. 

It is both morphologically and biologically very similar to th 
typhoid bacillus, to which it appears to be closely related. It is dis= 
tinguishable from the typhoid germ by several well-marked culture 
features, as well as by its pathogenic power. The points involved i: 
the differential diagnosis of the colon from the typhoid bacillus ar 
too intricate and numerous to be considered here. 

Recent studies, especially those of Welch, have shown that nc 
infrequently when the Bacillus coli communis finds access to the peri 
toneal cavity or other parts of the body where it does not belong, it i 
capable of inciting serious and even fatal disease. It may indue 
local suppurative inflammation, necrosis, and toxaemia. 

In the kidney, in the gall passages, in hgemorrhagic pancreatitis 
in appendicitis, and repeatedly in peritonitis, as well as in othe 
lesions, it has been found either alone or in association with othe 
germs. 

It would appear from the observations of Welch, 3 who found it i 
one or more of the organs of the body in thirty-three out of about tw 
hundred autopsies, that lesions of the mucous membrane of the intes 
tine, haemorrhage, ulceration, perforation, catarrhal and diphtheriti 
inflammation, strangulation, injury, etc., may open the way for ii 
access to various parts of the body. In some cases its presence ws 
associated with lesions, in some not. On the whole, it would seer 
that we are justified in regarding the colon bacillus as of occasion* 
pathogenic importance in man. The limitations of its significanc 
must be determined by further studies. 4 

1 Nicolaier, Centralb. f. Bak., October 13th, 1894, p. 601. 

2 Abel, ibid., Bd. xiii., Nos. 5 and 6, 1893. 

3 Welch, "The Bacillus Coli Communis: The Conditions of its Invasion of tl 
Human Body, and its Pathogenic Properties, " Medical News, December 12th, 189: 

4 For resume of properties of the Bacillus coli communis, with bibliography 
consult Darling, Boston Med. and Surg. Jour., November 15th and 22d, 1894. 



THE INFECTIOUS DISEASES. 261 

Micrococcus tetragenus. — This coccus growing in tetrads has 
been repeatedly found in cavities in the lungs in pulmonary tubercu- 
losis and in abscesses elsewhere. 

While its usual significance is not yet clear, it has been shown to 
be pyogenic. 

Bacillus pyocyaneus. — A pyogenic organism producing a green- 
ish fluorescence in culture media, is of occasional occurrence in sup- 
purative inflammation. It has been found in peritonitis and pericar- 
ditis, in broncho-pneumonia, in phlegmon, and under a variety of 
conditions in the gastro-intestinal canal. 1 

Bacillus proteus. — This germ is common in putrefying sub- 
stances, is frequently present in the intestinal contents; it grows in 
bizarre and irregular forms on gelatin and agar, and may apparently 
under certain conditions bo pathogenic. 

Bacillus aerogenes capsulatus. — Several observers have de- 
scribed an anaerobic, gas-forming bacillus occurring in emphysema- 
tous phlegmons, in gangrene, in peritonitis, and also after death in 
cases with early and abundant post-mortem gas formation in the 
tissues, especially in the blood vessels and in the liver (see page 614). 

It is probable that the gas-forming anaerobic bacillus above 
named, which was first described by Welch and Nuttall in 1892, is 
identical with some of those which under different names has been 
since described by various observers. 2 

1 Kossel, Zeitschrift f. Hygiene und Inf. Kr, , Bd. xvi., p. 368 ;&\soJakowski, ibid., 
p. 474. 

2 For a full consideration of this important micro-organism see Welch and Flexner, 
Journal of Experimental Medicine, vol. i., p. 5, 1896. 



ACTINOMYCOSIS. 

This disease is due to the growth in the body of a micro-organisn 
whose botanical position is not quite clear, but which seems to belong 
among the bacteria. This micro-organism, the actinomyces, appears 
to belong to one of the more complex groups of bacteria called th< 
Cladothricaceae, which develop in the form of branching filaments 
These filaments in actinomyces frequently separate into longer an( 
shorter rod-like or almost spheroidal segments. 

It may be grown on artificial culture media, flourishing best a 
body temperature. It at first develops in the form of delicate 




Fig. 105. — Actinomyces Bovis. 
Showing one of the yellowish masses of the parasite separated from the surrounding tissue. 



branching threads, the older cultures showing segments which 
resemble bacilli and cocci, and various bulbous, flask-like or club- 
shaped forms which appear to be the result of degeneration ("involu- 
tion" forms) (Fig. 105). Successful inoculations of cultures have 
been made in animals. This micro-organism grows in radiate 
masses, especially in the jaws of cattle, but is of occasional occur- 
rence in man. The fungous mass may form a large tumor in the 
jaw, b} 7 its own growth and by the formation of granulation tissue, 
which is apt to slough and spread, so that not only may the tissues of 
the tongue, pharynx, larynx, etc., be involved, but nodules of similar 
character may form in the gastro-intestinal canal, lungs, skin, etc. 
In man suppuration with necrosis and the formation of abscesses, 



THE INFECTIOUS DISEASES. 



263 



ulcers, and fistulpe may be the marked accompaniments of its growth 
in parts near the surface of the body. 

In the lungs the lesions may be essentially those of an acute 
general bronchitis or in the form of broncho-pneumonia (Fig. 106), 
with the formation of new tissue. Abscesses and cavities may form 
which extend into adjacent parts. The characteristic masses of 
the micro-organism may be found in the sputum in these cases of 
actinomycosis of the lungs. 1 

In intestinal actinomycosis nodular masses of new tissue with 




Fig. 106.— Actinomyces Growing in Human Bronchus. 
Tne bronchus is filled with a purulent exudate and its wall is becoming involved. 



ulceration may develop in the mucosa and submucosa. Metastases 
have been described. 

The fungus forms little yellow masses as large as a millet seed or 
smaller, which are scattered through the new-formed granulation 
tissue or mingled with the pus, giving the growths a very character- 
istic appearance. It is the peculiar radiate grouping of the filaments 
of the growth (Fig. 106) which gave rise to the name "ray fungus." 

1 For a detailed description of the lung lesions in actinomycosis, with general 
bibliography, see Hodenpyl, ''Actinomycosis of the Lung," New York Medical 
Record, December 13th, 1890. 



264 THE INFECTIOUS DISEASES. 

The disease is propagated from one animal to another by inoculation 
or by contact of the growth with a wound or an abrasion of the 
mucous membrane. The fungous masses may become calcareous. 

In the examination of sputum, faeces, pus, etc., for the presence 
of actinomyces, the naked-eye appearances may be of value, since 
the yellowish -white granules are often quite visible, especially on s 
black background. Suspicious masses may be teased and studied 
unstained, or stained by Gram's method. Sections of tissue contain- 
ing actinomyces may be hardened in alcohol, and sections stained by 
Gram's method with contrast eosin stain. 



ASIATIC CHOLERA. 

In some cases of cholera there are no marked changes to be found 
after death. Id no case are the lesions distinctive of this disease. 

If death occur during the invasion of the disease or in the stage 
■of collapse, the appearances may be as follows in the more marked 
cases : 

The bodies remain warm for some time, and the temperature may 
rise for a short time after death. The rigor mortis begins early and 
lasts for an unusually long time. The muscles sometimes exhibit a 
peculiar spasmodic twitching before the rigor mortis sets in, especially 
the muscles of the hand and arm. 

The Skin is of a dusky gray color, the lips, eyelids, fingers, and 
toes of a livid purple. The ends of the fingers are shrivelled, the 
cheeks and eyes fallen in. 

The Brain. — The sinuses of the dura mater are filled with dark, 
thick blood. The pia mater may be normal, or cedematous, or ecchy- 
mosed, or infiltrated with fibrin. The brain is usually normal, but 
may be dry and firmer than usual. 

The Lungs are retracted and anaemic, the pleura may be dry or 
coated with fibrin. 

The Heart is normal. 

The Peritoneum may be dry or coated with a layer of fibrin. 

The Stomach is usually unchanged, but may be the seat of ca- 
tarrhal inflammation. 

The Small Intestine. — There may be ecchymoses in the mucous 
membrane; the mucous membrane may be soft and cedematous; 
there may be general congestion, or the congestion may be confined 
to the peripheries of the solitary and agminated nodules, and these 
nodules may be swollen ; or there may be croupous inflammation and 
superficial necrosis. All these changes are regularly most marked at 
the lower end of the small intestine. There is apt to be post-mortem 
desquamation of the epithelium. The characteristic rice-water fluid 
may be found in the intestines after death, or instead of this dark- 
colored, bloody fluid. 

The Large Intestine is usually normal, but in some epidemics 
croupous inflammation occurs in a considerable number of cases. 



266 THE INFECTIOUS DISEASES. 

The Spleen may be soft. The Liver may show small areas of 
granular or fatty or hyalin degeneration. 

The Kidneys are often increased in size, with white and thick- 
ened cortex and congested pyramids. The epithelium of the cortex 
tubes may contain coarse granules and fat globules, or be necrotic. 
The tubes may contain cast matter and broken-down epithelium. 
These changes may be looked upon as being simply of a degenerative 
character or as the results of an acute degeneration from absorbed 
toxins. 

The Uterus and Ovaries may be congested and contain extra- 
vasated blood. 

If the patient do not die until the stage of reaction, the body does 
not preserve the same collapsed appearance, and there are often 
inflammatory changes in different parts of the body, especially in the 
larynx, the lungs, the stomach, and the intestines. 

According to the researches of Koch, which have been abundantly 
confirmed by others, there are constantly present in the small intes- 




Fig. 107.— Spirillum Cholera Asiatics:. 
From a culture. 

tines of cholera patients, during the early and active stages of the 
disease, characteristic curved rods which are not known to occur in 
the body under any other conditions, and which have been proved to 
cause the disease. These rods are from 0.8 to 2.0 t± long, and are 
sometimes slightly, sometimes considerably curved (see Fig. 107). 
When growing under suitable conditions, the individual rods are apt 
to cling together by their ends, forming S-shaped figures or spirils of 
considerable length. From the curved shape of the individuals they 
are also often called "comma bacilli;" but the organism appears to 
belong among the spirilla and is therefore called Spirillum cholerce 
Asiaticce (or "Cholera vibrio"). The spirilla may be present in 
moderate numbers in and beneath the mucous membranes of the 
intestine, and in very large numbers in the intestinal contents and in 
the dejections in the acute forms and early stages of the disease. 

In the process of their growth and multiplication in the intestinal 
canal they apparently produce a poisonous substance, the local 
action and absorption of which into the body fluids produce the symp- 
toms and lesions of the disease. The systemic effects appear to be in 



THE INFECTIOUS DISEASES. 267 

the nature of a septic intoxication. The cholera bacillus may retain 
its vitality for a considerable period in water, and on moist substances, 
such as damp linen, earth, and vegetables, it may increase in num- 
bers with great rapidity. 

A temperature of from 30° to 40° C. is most favorable for its 
growth. At about 16° C. proliferative activities cease, but the germs 
are not killed by — 10° 0. They are readily killed by drying, and 
the presence of acids is very inimical to their growth. 

There is not sufficient evidence that they form spores, and their 
period of life is short. 

The cholera bacillus is readily cultivated on artificial culture 
media, such as gelatin, agar, milk, beef tea, potatoes, etc. In fluids 
it is capable of performing active movements and is furnished with 
flagella. 

While it may be readily stained by the ordinary methods when 
present in the dejecta, its morphological characters are not absolutely 
distinctive, since several forms of curved bacilli belonging to the 
same group and closely resembling the cholera vibrio have, under 
varying conditions, been found in the dejecta and in the mcuih. 

It is often of the highest importance to determine, at the earliest 
possible moment, whether or not a suspected case be one of Asiatic 
cholera or some other form of acute intestinal disorder, so that in 
the former case the proper measures may be instituted to prevent 
the spread of the disease. The characters which are developed in 
cultures of the cholera bacillus enable an expert biologist to distin- 
guish this organism from all other known forms. 

But the scope of this work does not permit a detailed description 
of the cultural peculiarities of the germ. Nor should the responsi- 
bility of such determinations be assumed without adequate prelim- 
inary laboratory experience. 

By taking together the morphological and biological characters, it 
is possible, usually on the second or third day, to determine whether 
the intestinal contents of a, suspected case do or do not contain the 
bacillus of Asiatic cholera. 

The cholera vibrio, both in the dejecta and in pure cultures, is 
readily stained by the ordinary anilin dyes. The results of animal 
experiments with the cholera germ are not in themselves decisive in 
determining its relationship to this disease, since animals do not react 
in its presence as man does. 

However, the constant occurrence of tbis organism in Asiatic 
cholera, its absence under other conditions from the body, and the 
accidental laboratory infections which have several times occurred in 
men handling pure cultures of the germ, leave no doubt as to its 
instrumentality in the causation of the disease. 



268 THE INFECTIOUS DISEASES. 

The disease is communicated from one person to another by th< 
pollution of food or drink with the discharges which contain th< 
virulent germs. 

The results of a large amount of work which has been done, look 
ing toward a practical artificial immunization of man against Asiatic 
cholera in the East have not yet been sufficiently definitely formulated 
to permit a final judgment as to its value. 1 

1 For the details of his researches on Asiatic cholera, see Koch's report, " Arbeitei 
a. d. kaiserlichen Gesundheitsamte, " Bd. iii. , 1887. Consult also Shakespere's "Re 
port on Cholera in Europe and India, " 1890. 

For bibliography of recent studies see Dunbar, "Ergebnisse der allg. Aetiologie 
der Menschen- u. Thierkrankheiten, " 1896, p. 804. 



RELAPSING FEYER. 

{Typhus recurrens; Famine Fever: Spirillum Fever; Seven Day 

Fever.) 

The lesions which may be present in this disease are not distinc- 
tive of it. 

Its distinguishing feature, apart from symptoms, is the presence 
in the blood at certain periods of the specific micro-organism. 




Fig. 108.— Spirochete Obermeieri in the Blood in a case of Relapsing Fever. 



The Skin may be jaundiced ; it may be mottled by extravasations 
of blood. 

The Brain and Spinal Cord are unchanged. 

The Pharynx and Larynx may be the seat of catarrhal or croup- 
ous inflammation. 

The Lungs. — There may be bronchitis, broncho-pneumonia, lobar 
pneumonia, hypostatic congestion, and pleurisy. 

The Heart is often soft and flabby, with degeneration of its mus- 
cular fibres. There may be ecchymoses in the pericardium. 



270 THE INFECTIOUS DISEASES. 

The Stomach and Small Intestine may be congested ; there may 
be ecchymoses in the mucous membrane; there may be catarrhal 
inflammation. 

The Colon may be the seat of catarrhal or croupous inflammation. 

The Mesenteric Nodes may be swollen. 

The Liver is often enlarged and the hepatic cells are swollen and 
granular. 

The Spleen is large and soft. The change in its consistence is so 
marked that the spleen may rupture spontaneously during life. The 
spleen may also contain infarctions of different sizes; some are red, 
some yellow, some necrotic. Those which are necrotic may give rise 
to a local or general peritonitis. 

The Kidneys show the lesions of parenchymatous degeneration. 

Degenerative and hyperplastic changes in the medulla of the bones 
have been described. 

Bacteria. — In the blood of all parts of the body during the febrile 
attacks may be found, in very large numbers, a long, slender spiril- 
lum called from its discoverer Spirochete Obermeieri. It disappears 
from the blood during the afebrile intervals. The organism is from 
14 to 40 [J- in length, and performs rapid, undulating movements 
(Fig. 108) . The inoculation of healthy men and of monkeys with the 
blood of relapsing-fever patients which contains the bacteria induces 
a similar disease. Pure cultures have not as yet been made of these 
bacteria, but for the reasons indicated, and since the organism has 
never been found except in connection with the disease, there is every 
reason for believing that the Spirochsete Obermeieri is the cause of 
relapsing fever. 



VARIOLA. 

(Small-pox.) 

Small-pox is an acute, readily communicable, infectious disease, 
especially characterized anatomically by an inflammation of the skin 
which passes through a series of more or less distinctive phases of 
papule, vesicle, pustule, with a final drying of the exudate and 
necrotic tissue constituting the crust. 

Various phases of the exanthem are used to designate forms of 
the disease. 

Secondary lesions are diffuse suppurative . inflammation of the 
skin, inflammations of the mucous membrane, haemorrhages in 
various parts of the body, and acute degeneration of the kidney, liver, 
and spleen. 




Fig. 109.— A Small-pox Vesicle of the Skin. 



The skin lesion shows in general at first circumscribed areas of 
inflammation above the ends of the papillae, with the development of 
a fluid-filled reticulum, so that vesicles are formed (Fig. 109). These 
at first contain a clear fluid, but by the gathering of pus cells the fluid 
becomes turbid and accumulates to form a pustule. Hand-in-hand 
with these changes the papillae and adjacent layers of the corium may 
become infiltrated with cells. The contents of the pustules and the 
necrotic tissue above dry and form the crusts. When the changes 
are largely confined to the epidermis the lesion may leave no deform- 
ity. But if the changes in the cutis are considerable, cicatricial 



272 THE INFECTIOUS DISEASES. 

tissue may form, leaving scars. The association of local hsemor 
rhage with the above changes gives rise to the haemorrhagic fora 
of exanthem. 

Various micro-organisms, both bacteria and protozoa, have beei 
described as occurring in the local skin lesions of small-pox, but th< 
cause of the disease is still unknown. 

The protection conferred by a successfully weathered attack o 
small-pox is one of the most striking examples of this form of ac 
quired immunity (see page 179). The more recent views of the im 
munity conferred by vaccination against small-pox is based upon th< 
demonstration that the disease variola in man and the disease vaccina 
in the bovine species are the same, and not different, as was formerl} 
believed ; that the disease in the cow is only a modified form of th( 
human disease. The effect of the passage of the unknown but cer 
tainly existing micro-organisms through the insusceptible bovine— 
thus runs the rationale in the new light — is to so diminish the viru- 
lence of the germ that by its subsequent inoculation in man im- 
munity is produced without the profound disturbance which infection 
with a germ of unmitigated virulence would involve. 



SCARLET FEVER. 

{Scarlatina.) 

This is an infectious, readily communicable disease characterized 
"by a diffuse skin eruption, and frequently accompanied by inflam- 
mation, either catarrhal, croupous, or gangrenous, of the tonsils, 
pharynx, and larynx. 

There may be acute hyperplasia or suppuration of the cervical 
lymph nodes. There is very frequently an acute exudative or an 
acute diffuse nephritis. The spleen may be enlarged. Broncho- 
pneumonia, endocarditis, and pericarditis may occur. 

The exanthem or skin eruption in scarlatina is a simple dermatitis, 
as the result of which the papillae and subpapillary stratum become 
infiltrated with fluid or leucocytes, or both, the leucocytes being 
gathered especially about the blood vessels. There may be small 
haemorrhages, and the acute phase of the inflammation is followed by 
an increased production of epithelium and an exfoliation of the super- 
ficial layers. These lesions of the skin are, excepting the haemor- 
rhages, very slightly marked after death. 

That the disease is due to some form of micro-organism there can 
be no doubt. The exact nature of this organism is not yet known. 
The acute nephritis so often present appears to be due to some poison 
produced in the body during the disease. One of the most marked 
features of the disease is the predisposition which it entails to the 
incursions of pathogenic germs other than those which we believe to 
cause the disease itself. Thus an infectious croupous inflammation 
in the mouth, tonsils, pharynx, larynx, and trachea, due to a strepto- 
coccus (see page 205), is a frequent complication. True diphtheria 
•due to the Loffler bacillus is also prone to establish itself upon the 
vulnerable inflamed mucous membranes. 

So also the frequently associated pneumonia, the inflammatory 
hyperplasia and suppuration of the lymph nodes, suppurations in 
various parts of the body, the endocarditis and pericarditis which are 
not uncommon, may all be due to a secondary infection with the 
pyogenic cocci. 
23 



MEASLES. 

A readily communicable infectious disease, the most prominei 
features of which are an intense hypersemia with inflammation c 
the skin, associated with catarrhal inflammation of the mucous men 
brane of the air passages. The inflammation of the skin is anatoir 
ically of the same general type as that in scarlatina. Acute degenei 
ation of the kidney or acute exudative nephritis may follow. Tb 
more common secondar} T lesions are broncho-pneumonia, pseudc 
membranous inflammation of the pharynx and larynx, suppurativ 
inflammation in various parts of the body, and diphtheria. Thes 
complications, as in scarlatina, are doubtless, in part at least, due i 
secondary infection with other germs than those causing the diseas 
itself. 

The micro-organism causing measles is not known. 1 

1 Canon and Pielicke in 1892 (Berliner klin. Wochenschrift, April 18th, No. U 
recorded the discovery in the blood in fourteen cases of measles of a very sma 
bacillus, about as long as the radius of a red blood cell, but varying considerably i 
size. It is best stained with Czenzynski's solution (p. 68), or with a solutio 
containing one-half the amount of eosin. Sometimes the staining is uniform, som< 
times the middle portion is paler. These bacilli were sometimes abundant, somi 
times scanty in the blood, lying singly or in heaps. Meagre cultures were obtaine 
in three cases in beef tea. They did not seem to grow on the ordinary solid medif 
Bacilli similar in form were found in the exudate from inflamed mucous membrane 
in measles. The observations of these writers are interesting and suggestive, bv 
until they shall have been confirmed by others and been greatly extended nothin 
can be regarded as established regarding the etiological significance of the germs. 



TYPHUS FEVER. 
{Hospital Fever; Spotted Fever; Jail Fever; Ship Fever; etc.) 

This disease has not, so far as we know, any characteristic lesion 
save the petechial skin eruption ; but yet after death we may find a 
number of morbid conditions, such as are common to many of the 
infectious diseases. 

The entire body has a tendency to rapid putrefaction. 

The blood is often darker and more fluid than in other diseases. 

The voluntary muscles may undergo waxy and granular degener- 
ation. 

The brain and its membranes may be congested. 

The mucous membrane of the pharynx and larynx may be the seat 
of catarrhal or croupous inflammation. 

In the lungs there may be bronchitis, broncho-pneumonia, or hy- 
postatic congestion. 

The walls of the heart may be soft and flabby. 

The agminated nodules of the ileum, and the mesenteric nodes 
may be a little swollen. 

The spleen is often large and soft. 

The kidneys and liver are frequently the seat of parenchymatous 
degeneration. 

The nature of the infective agent in typhus is unknown. Several 
observers have recorded the finding of micro-organisms of one kind 
or another in the disease, but proof that any of these have causative 
relationship to the disease has not yet been furnished. 1 

1 Bran nan and Gheesman, "A Study of Typhus Fever, " Medical Record, June 
25th, 1892. 



HYDROPHOBIA. 
{Babies.) 

The lesions which have been found in this disease are not constant 
nor are they characteristic. Though well marked in some cases, 
they are but very slightly developed in others. 

The lesions, when present, are apt to be most marked in the 
medulla oblongata and pons, but they may be present in the cord 
(Fig. 110). They consist of small haemorrhages, accumulation of 











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^£;?S'!^ : y ; ' : ; v fr •■:!;■ , . y.: • x V- .>;. -S^ 
" "*' - . • ,- <&• '" 

Fig. 110.— Section op Spinal Cord from a Case of Hydrophobia. 
Showing large accumulation of leucocytes about the blood vessels, both in the gray and' in the 
white matter. (From a specimen prepared by Van Gieson. ) 

leucocytes about the blood vessels in the perivascular lymph spaces 
and around the ganglion cells, and of thrombi in the smaller blood 
vessels, and of degeneration of the ganglion cells especially in the 
spinal cord. 1 None of these lesions are, however, pathognomonic of 
this disease. 

1 Babes, Annales de l'lnstitut Pasteur, April, 1892, and August, 1895. 
For an account of lesions in experimental rabies consult Golgi, Berliner klku 
Wochenschrift, April 2d, 1895. 



THE INFECTIOUS DISEASES. 



277 



While there is every reason for believing that hydrophobia is due 
to the introduction into the body of some special form of micro- 
organism, and while the recent researches of Pasteur and others have 
brought to light many interesting and important facts regarding the 
general nature and distribution in the body of the infectious agent, 
nothing is yet definitely known about the particular organism which 
induces the disease. 

It is known that the infectious agent is in the saliva and salivary 
glands of rabid animals, and that it may be present in the saliva of 
the dog two or three days before the symptoms of the disease are 
manifest. It is not present in the blood, but seems to be especially 










ee 



if 



Fig. 111.— Hydrophobia, Transverse Section op Small Blood Vessels in the Spinal Cord. 
From the same case as Fig. 110, more highly magnified. Showing accumulation of leucocytes 
and proliferation of connective-tissue cells in the adventitia of the vessels. 



concentrated in the central nervous system and particularly in the 
medulla oblongata. 

Notwithstanding the total ignorance of the micro-organism con- 
cerned in inciting hydrophobia, his genius in wise experiment en- 
abled Pasteur to discover and to establish a method for artificial 
immunization against the disease which has proved most beneficent. 

After obtaining a virus of definite intensity, which was accom- 
plished by a series of inoculations beneath the dura mater in rabbits 
of portions of the spinal cords of rabid animals, it was found that 
by drying spinal cords of definite and high virulence in the air, with 
due protection against aerial contamination, the virulence diminished 



278 THE INFECTIOUS DISEASES. 

day by day. With virus thus obtained of virulence ranging from 
that which is practically inert to that of the utmost potency, it has 
been found possible to safely accustom both animals and men to the 
presence of amounts of hydrophobia virus contained in the spinal 
cord emulsion, which under ordinary conditions would prove speedily 
fatal. In other words, it has been found possible to confer artificial 
immunity against the disease. 

This process occupies several days, and immunization must be 
completed before the disease has begun to manifest itself ; but as the 
incubation period in hydrophobia is a long one, it has been possible, 
in a large and increasing number of cases, to save the lives of persons 
bitten by rabid animals. 

In view of the importance of diagnosis, in dogs which have died 
or have been killed under suspicion of rabies, the spinal cord and 
medulla should be saved. Portions of the fresh medulla in emulsion 
water should, if possible, be inoculated beneath the dura mater of 
two healthy rabbits and the development of rabic paralysis and other 
symptoms observantly awaited. 

Other portions of the medulla and cord should be hardened in 
Miiller's fluid and alcohol, and carefully examined especially for small 
perivascular accumulations of leucocytes. The existence of these in 
the medulla and cord of an animal suspected of rabies will go far 
toward confirming the suspicion. 



YELLOW FEVER. 

This infectious disease is without characteristic lesions save for 
the haemorrhages and pigmentation in the skin. The following con- 
ditions are, however, frequently present after death : 

Rigor mortis is marked and occurs early. 

The Brain and its meninges are usually congested. 

The Skin is of a yellow color from the presence of bile pigment, 
and may be mottled by ecchymoses. 

The Heart is of a pale or brownish-yellow color. Its muscular 
fibres may be the seat of fatty degeneration. 

The Lungs may be congested. 

The Stomach often contains the characteristic black fluid due to 
altered blood pigment which is vomited during life. Its mucous 
membrane may be congested, softened, and is sometimes eroded. 

The Intestines are dark-colored, often distended with gas, and 
sometimes contain blood. 

The Liver in the earlier stages of the disease may be intensely 
congested. More frequently it contains but little blood, is of a light- 
yellow color, and the hepatic cells show the changes of an intense 
acute degeneration, much more marked than are found in any other 
disease except acute yellow atrophy of the liver. The gall bladder is 
apt to be contracted. 

The Spleen shows no marked changes. 

The Kidneys present the lesions of an intense form of parenchy- 
matous degeneration. Tubules usually contain masses of hyalin 
material. 

While its mode of occurrence and the characters of its symptoms 
and lesions afford a strong presumption that yellow fever is an acute 
infectious disease, none of the various studies which have been made 
upon its etiology have as yet revealed the presence of any micro- 
organism to the action of which it can be fairly attributed. 1 

1 The studies of Sternberg on the "Etiology and Prevention of Yellow Fever, " 
published in the form of a Government report in 1890, contain the result of a great 
deal of research by modern methods, and should be consulted for a full exposition of 
this disease and its lesions. 



THE MALARIAL FEVERS. 

The characteristic lesions of malarial poisoning are certain changes 
in the blood, the spleen, and the liver. 

In the more intense and acute form of malarial poisoning the 
blood contains numerous particles of black or brown pigment, which 
are either free or embedded in cells resembling the white blood cells 
or in the endothelium of the blood vessels. After death this pigment 
is found in the blood vessels throughout the body, but is most abun- 
dant in the blood vessels of the liver (see Fig. 293) and spleen. 
These organs are then usually of large size and of a peculiar brown 
or black color. 

In some of these severe cases there are also extravasations of blood 
from the mucous membranes and in their substance. There may also 
be general jaundice. Focal necroses in the viscera similar to those 
occurring in other infectious diseases have been described. 

In the milder and more protracted cases of malarial poisoning the 
composition of the blood is altered and the patient may become pro- 
foundly anaemic. The spleen may become the seat of chronic inter- 
stitial inflammation with pigmentation (see Fig. 305). The liver 
may exhibit the changes of chronic interstitial hepatitis. 

The attempts to establish a causative relationship between the 
various forms of bacteria which from time to time have been found 
in the bodies of persons who are the victims of malarial poisoning, 
and the symptoms and lesions of the disease, have all been unsuc- 
cessful. 

On the other hand, a large number of careful studies by various 
observers have led to the general belief that the disease is due, 
not to vegetable, but to intercellular animal organisms which are very 
constantly found in the blood of affected persons. 

These organisms, which belong among the protozoa, may be ap- 
propriately called the hcematozoa of malaria. They are, however, 
often called the Plasmodia malariae. 

In brief, the facts upon which this belief rests are as follows: 
The blood of those suffering from malarial poisoning may contain, 
which the blood under other conditions does not, one or more of the 
structures which are shown in Fig. 112. 



THE INFECTIOUS DISEASES. 



281 



1. Inside of the red blood cells may be found colorless bodies, 
sometimes occupying a small part, sometimes nearly filling the cell. 
These bodies may or may not contain pigment granules. They may 
exhibit amoeboid movements (a and b). They are called the amoe- 
boid bodies. 

2. Colorless discoidal bodies, usually a little larger than the red 
blood cells, which contain pigment particles, sometimes scattered 
irregularly, sometimes grouped toward the centre. These are be- 
lieved by some observers to be the later developmental stages of the 




Fig. 112.— The ILematozoon of Malaria (Plasmodium Malarle) in the Blood. 

a, unpiginented amoeboid body in a red blood cell; 6, pigmented amoeboid body; c, colorless 
discoidal body with pigment; d, segmenting body; e, fragments of segmenting body; / and g, 
crescentic bodies; h, flagellate body, a, 6, d, e,f, g are drawn from specimens of malarial blood 
prepared by Dr. Walter James; c and h are drawn after sketches by Dr. James. 



amoeboid bodies, which have increased in size at the expense of the 
red blood cells. A grouping of pigment granules indicating segmen- 
tation is sometimes seen in these bodies. These are called the en- 
cysted bodies (c). 

3. Bodies, about the size of a red blood cell, which are composed 
of a congeries of irregularly rounded structures grouped about a 
central mass of pigment. These are called segmenting bodies or 
rosettes (d). 

4. Smaller isolated or clustered structures which are apparently 

23 



282 THE INFECTIOUS DISEASES. 

the result of the breaking apart of the segmenting bodies, as seen at 
e. Often called spores. 

5. Crescentic bodies containing a central mass of pigment (f 
and g). 

6. Bodies, smaller than a red blood cell, which are actively mobile 
and are furnished with one or more flagella at one side — h, flagel- 
late form. These are the main forms which have been described. 

The amoeboid forms are apt to occur in the acute stages of the 
disease, the crescentic forms in the chronic stages. The segmenting 
bodies are apt to be present immediately before or during the chill ; 
the pigmented amoeboid bodies, according to James, are present at all 
times, but are most numerous during and before the paroxysms. In 
general, it may be said that the number of these bodies is proportional 
to the gravity of the case. The amoeboid forms disappear shortly 
after the administration of quinine, while the crescentic bodies often 
persist for a considerable time under the same conditions. 

It is believed that these various forms represent phases in the 
development of one or more varieties of the parasite. The cycle of 
development appears to be brief — in the organism of tertian fever 
about forty-eight hours — in that of quartan about seventy-two hours 
— and quickly recurrent; so that paroxysm may follow paroxysm, 
the height of each corresponding to the sporulation or segmentation 
of the parasite. 

If the body be infected with a single brood or growth of the para- 
sites the paroxysm will be apt to recur regularly, in accordance with 
a simple type; but should two or more broods or groups, reaching the 
period of sporulation at different times, be present, the paroxysm will 
recur with greater frequence and at less regular intervals. 

While much is known about the hsematozoa of the various phases 
of malarial fever, much study is still necessary for the completion of 
their life histories, and much more light is needed on the way in 
which the parasites produce their effects in the body, aside from the 
destruction of the blood cells, to which pigmentation is due. All 
attempts to cultivate the organisms under artificial conditions have 
thus far failed. While by the direct transference of malarial blood 
from animal to animal and from man to man the disease may be 
induced, under the ordinary conditions of life it is not communicable ; 
nor do we know the habitat of the organism in nature or its portals 
of entry to the body. 

Whatever its full etiological significance or its life history, its 

discovery in the blood, even with our present knowledge, since it is 

unknown except in malarial disease, is of great diagnostic value in 

doubtful cases. 1 f 

1 For bibliography and a resume of the work already done on this subject con- 



THE INFECTIOUS DISEASES. 283 

Method of Examination. — The fresh blood taken from a finger 
prick may be examined in thin layers on the warm stage with one- 
twelfth oil immersion. 

For stained preparations the method described on page 88 may 
~be followed, or, after spreading and fixing the blood film as above, 
the cover may be floated, specimen side down, for from ten to fifteen 
minutes in Czenzynski's fluid : 

Aqueous Methylen Blue, saturated solution 20 c.c. 

One-half-per-cent solution of Eosin in seventy - 

per-cent Alcohol " 10 " 

Water 20 " 

Hinse in water and mount in balsam. In this way the plasmodia 
.and the nuclei of the leucocytes are stained blue, the red blood cells 
and eosinophile granules red. 

suit TJiayer and Hewetson, "The Malarial Fevers of Baltimore, " etc., Johns Hopkins 
Hospital Reports, vol. v., 1895, pp. 5-215. 

Also Barker, " A Study of Some Fatal Cases of Malaria, " ibid. , pp. 221-270. 






PHARYNGO-MYCOSIS LEPTOTHRICA. 

Certain filamentous micro-organisms called Leptothrix, and be- 
lieved by some observers to be more closely allied to the algse than to 
the fungi, are of common occurrence in the mouths of healthy per- 
sons. Occasionally, however, a persistent recurrent attack of " &ore 
throat " with local tenderness and sometimes cough and fever, are 
associated with the growth of masses of leptothrix in the crypts of 
the tonsils, at the base of the tongue, on the walls of the pharynx, or 
in the nose or superior portion of the oesophagus. 

The leptothrix masses or colonies form thick whitish pellicles or 
patches which may be superficial, or in the tonsils may extend deep 
into the crypts. These masses are usually firmly adherent, often 
leave bleeding surfaces when removed, and the growth is apt to per- 
sistently recur. 

Microscopical examination of removed portions of the growth 
show tufts and bundles of the thread-like micro-organisms, growing 
among or directly out from flat epithelial cell masses and mingled 
with various other forms of micro-organisms, mostly cocci and short 
bacilli. 

There may be overgrowth of epithelium and collections of leu- 
cocytes in and about the leptothrix masses. 

In sections of the tissue or in teased fragments treated with iodin 
(Lugol's solution) the leptothrix threads are readily differentiated 
from the tissue elements and from other micro-organisms, by their 
dark color. 1 

1 For further details and bibliography, consult Campbell, Medical News, April 
4th, 1896. 



INFECTIOUS DISEASES OF ANIMALS. 

The study of comparative pathology is of great and increasing 
importance, and already much light has been thrown on the nature 
of human diseases by the study of the diseases of the lower animals. 

While this is true of pathology in general, it is of especial signifi- 
cance in the study of the infectious diseases of the lower animals, not 
only as they occur spontaneously, but also in fields of experimental 
research. 

The scope of the book does not permit of a more than occasional 
reference to animal diseases, but the reader may consult : Nocard and 
Leclainche, " Les Maladies Microbiennes des Animaux," Paris, 1896, 
aud the translation by Dinwiddle of the "Manual of Veterinary 
Microbiology," by Mosselman and Lienaux, 1894. 



TUMORS. 



SECTION" I. GENERAL CHARACTERS. 

Tumors are composed of the same types of tissue as those normally 
existing in the body, and from the latter they are derived by a pro- 
liferation of pre-existing cells. The tissues of tumors may be similar 
to those of the part in which they grow, when they are called ho- 
mologous ; or they may be dissimilar, and are then called heterolo- 
gous. Tumors are not only analogous to the normal tissues of the 
body in structure, but their life history transpires under the same 
general laws of nutrition, growth, reproduction, etc. With this im- 
portant difference, however : that while the normal tissues, serv- 
ing as they do a definite purpose in the organism, are closely limited 
in their growth and minute characters by physical and other condi- 
tions which determine the uniform development and correlation of 
various parts, the tissues of tumors exhibit a certain lawlessness in 
growth, structure, and life history which gives them a distinctive 
character while not removing them from the physiological types. 
Thus in the Chondromata 1 the tissue, while distinctly cartilaginous 
in type, presents itself not only in places where it does not belong, 
but may show a tendency to the development of fibres in one part of 
its basement substance, while another may be distinctly hyalin, or 
another soft and almost gelatinous. The cells also are apt to ex- 
hibit great lack of uniformity in size, shape, and grouping. The 
lawlessness in tumor tissues is shown in their tendency, under cer- 
tain conditions, to change from one form into another, as from fib- 
rous tissue into bone. 

Tumors are supplied with blood vessels which grow into them 
from adjacent healthy parts, jiist as they do into granulation tissue, 
so that they may finally possess a more or less independent vascular 
system of arteries, capillaries, and veins. They are furnished with 
lymph vessels and some of them with nerves. The cell division by 

1 Tumors are designated by the termination oma (plural omata). 



TUMORS. 287 

which tumors grow exhibits the same minute phenomena as does 
cell division in normal tissues (see page 72). Tumor tissues are sub- 
ject to the same degenerative changes as other tissues ; they may 
become fatty or calcified, ulcerated, gangrenous, pigmented, etc. 
By necrotic changes a tumor may be largely destroyed, but com- 
plete obliteration rarely occurs in this way. They are liable to un- 
dergo the ordinary inflammatory changes, granulation tissue may 
form in them, and abscesses and cicatrices. 

The rapidity of growth of tumors varies greatly ; some grow 
very slowly indeed and may change but imperceptibly in size and 
appearance for years, while others, on the other hand, grow so fast 
that they do not acquire solidity, and their elements remain in an 
incompletely developed condition and are thus more liable to de- 
structive changes than normal tissues are. In healthy tissues the 
blood vessels are supported by surrounding elements, which aid them 
in sustaining the blood pressure from within. In rapidly growing 
tumors this external support is often lacking, and, as the walls of 
the blood vessels are themselves badly formed, the result is that the 
walls are apt to become pouched or aneurismal, and they often burst, 
giving rise to larger or smaller interstitial haemorrhages. 

Tumors have various shapes : nodular, tuberous, fungoid, poly- 
poid, papillary, dendritic, etc. 

Tumors may occur singly or in greater or less numbers in the same 
or in different parts of the body. If they are multiple they may 
have occurred simultaneously or at different times as independent 
structures. Or multiple tumors may occur as the result of the dis- 
semination in the body, from a primary tumor, of cells which form a 
starting point for new tumors. Many tumors are sharply circum- 
scribed, may be even encapsulated, and influence surrounding parts 
only by the pressure which they exert upon them. In this way they 
may cause displacement, atrophy, or necrosis ; they may, by pressure 
on neighboring vessels, cause oedema, thrombosis, etc. ; they may in 
the same way cause dislocation and caries of bones. 

Tumors may grow largely by increase of elements within them, 
thus simply expanding ; this is called central growth. They may 
grow in part or largely at the surf ace — peripheral growth. In this 
case the growth may be a direct, continuous enlargement of the mass 
at or near the periphery, or it may be by the formation of secondary 
nodules near the primary growth, which, gradually enlarging, finally 
coalesce with the latter, forming a part of the nodular tumor. This 
mode of enlargement is called discontinuous peripheral groivth, 
and is due to the dissemination of cells from the mother tumor into 
the adjacent tissue through the blood or lymph channels, and their 
proliferation at the points of lodgment. This dissemination may 



288 TUMORS. 

occur by the agency of blood or lymph currents or by the amoeboid 
movements of the cells. 

It is not yet certain whether the new cells which are produced in 
tumors are altogether the result of the proliferation of the primary 
tumor cells, or whether the ordinary tissue cells of the part, connec- 
tive-tissue cells, white blood cells, etc. , may undergo transf ormatior 
and proliferation under the influence of the characteristic cells of the 
tumor. It is not unlikely that both modes of increase occur, although 
the former is probably the more common and important. Some 
tumors increase by an infiltration of surrounding tissues, whose ele- 
ments they gradually replace. In certain tumors the old tissue of 
the part in which they grow may remain with its vessels and form a 
sort of matrix whose interstices are infiltrated with the new tumor 
tissue. The irritation of the tumor may induce inflammatory new 
formation of tissue of the old matrix about or within the tumor. 

But all tumors are not limited to that part or region of the body 
in which they first occur. Sooner or later secondary nodules re- 
sembling the first may be found in the most distant parts of the 
body, sometimes singly, sometimes in great numbers. These may 
grow like the parent tumor, and themselves form foci for new dis- 
seminations. 

This dissemination of tumors is one of the most important ele- 
ments of malignancy, and is called metastasis, the secondary tumors 
being called metastatic tumors. This occurs by the transportation 
of tumor cells through the blood or lymph channels. Since the 
tumor itself may be filled with new and badly formed blood and 
lymph vessels, and its structures be in close contact with the vessels 
of the tissue in which it grows, the cells of the primary tumor may, 
by ulceration through, or by atrophy of, the walls, readily find their 
way into the lumen of the vessels and be swept away by currents as 
emboli, and, finding lodgment, proliferate and grow, forming sec- 
ondary tumors; or the proliferation may occur in the vascular endo- 
thelium itself, when the formation of emboli is easy to understand. 
When carried through the lymph vessels the tumor cells may for 
some time be kept from the larger channels and from general dissemi- 
nation by lodgment in the lymph nodes, where they may establish 
independent tumors. The parts of the body in which metastatic tu- 
mors are most apt to form depend, of course, upon the situation of the 
primary tumor and the distribution of the vascular channels through 
which dissemination occurs. 

The tumors in which metastasis is most apt to occur are, as a 
rule, those which grow rapidly, are vascular and succulent, and con- 
tain many cells. 

Not less variable than the size, mode of growth, and structure of 



TUMORS. 289 

tumors is their significance in the organism. Surgeons have in the 
past, and to a certain extent still do classify tumors, for practical 
purposes, as malignant and benign, and for a long time malignant 
tumor and carcinoma were synonymous terms. Now we know that 
other tumors as well as carcinomata are malignant, and, furthermore, 
contrary to the former belief, that malignancy does not depend upon 
any specific extra-cellular agent in the tumor. If we mean by a 
malignant tumor one which may cause death, any tumor may be 
malignant if growing in the right place. Thus a simple fat tumor, 
by pressing on the trachea, may cause suffocation, and any tumor 
may secondarily cause death by haemorrhage or septicaemia. The 
real signs of malignancy in a tumor are: 1. Invasion of adjacent 
tissues by eccentric or peripheral growth. 2. The tendency to local 
recurrence after removal. 3. The formation of metastases. 4. A 
tendency to interfere with the nutrition and general well-being of 
the body, which may give rise to a condition known as cachexia. 
The modes of invasion of surrounding tissues and the formation of 
metastases have been considered above. The tendency to local re- 
currence after removal is probably, in most if not all cases, due to 
the incomplete removal of the peripheral infiltrating cells. These 
may be very few in number and lacking in characteristic structural 
features, but are none the less endowed with the capacity of prolifera- 
tion and development into a new and similar tumor at or near the 
seat of the extirpated one. The infiltrating peripheral cells may re- 
main dormant for a long time after an operation, or may imme- 
diately commence to grow. The mere fact that a second tumor de- 
velops in the place of one removed does not imply malignancy, since 
it may result from the same mechanical cause which produced the 
first, as in the case of certain carcinomata of the lip induced by the 
mechanical irritation of a pipe. 

The drain upon the system by the rapid growth of a tumor, to- 
gether with the absorption from it into the body of deleterious putre- 
factive materials, from sloughing, ulceration, and degeneration, may 
give rise to fever and other constitutional disturbances. Or they 
may induce feebleness, anaemia, and that general impairment of the 
nutritive functions of the body known as cachexia. This condition 
is frequently rendered worse by the mental status of the patient in 
the presence of such a traditional object of alarm. 

It should be remembered, however, that so long as they are local- 
ized and have not undergone degenerative changes, even the most 
malignant tumors do not usually give rise to a cachexia, since the 
drain upon the nutritive powers of the system by their simple growth 
is not, under ordinary conditions, very considerable. When the 
system is deteriorated by the absorption of septic materials from 



£90 TUMORS. 

tissue degeneration, however, this may become a very important 
factor. 

This condition of cachexia, so evidently secondary to the growth 
and degeneration of the tumor, was formerly termed a dyscrasia or 
diathesis, and was supposed to precede and induce the growth of 
malignant tumors, particularly cancers. 

It is further to be noted that the fragments of tumors which have 
found access to the veins may act as simple emboli and produce im- 
mediate death or simple metastatic abscesses. 

It was formerly supposed, when the doctrine of the specific nature 
of tumors prevailed, that the cells of malignant tumors, particularly 
of carcinomata, had a characteristic structure and appearance, and 
that by the examination of single or of a few separated cells the na- 
ture of the tumor could be determined. From the above considera- 
tions it will be evident, as all tumor cells have their prototypes in 
the normal body, that therefore there is nothing pathognomonic in 
the appearances of single cells. It is by a study of the general struc- 
ture and of the topography of tumors, as well as of the characters 
of the individual cells, that we are enabled to determine their nature. 
And even then we must often bring to our aid the clinical history and 
gross appearances of the growth before we can arrive at a definite 
conclusion. We may, indeed, sometimes, aided by the clinical his- 
tory or gross appearances, be able, by the microscopical examination 
of scrapings from a tumor or of fluids from an internal cavity in 
which it is growing, to form a reasonable conjecture regarding its 
nature. 

As a rule, the peripheral portions of the more rapidly growing 
tumors are best adapted for microscopical examination, because here 
secondary degenerative changes are less likely to have occurred than 
in the central parts. 

THE CAUSE OF TUMORS. 

In regard to the causation of tumors our actual knowledge is still 
very meagre. In a certain number of cases mechanical influences 
are undoubtedly sufficient inciting causes. In other instances hered- 
ity is an important factor. But to both of these influences too much 
importance has been attributed in former times. The most recent, 
and to a certain extent plausible, hypothesis, and one which most sat- 
isfactorily accounts for the occurrence and character of many tu- 
mors, is that of Cohnheim, called the hypothesis of the embryonal 
origin of tumors. This is to the effect that all true tumors are due 
to faulty embryonal development ; that certain embryonal cells of 
various kinds, in the course of the development of the body, are 



TUMORS. 291 

superfluous, or become displaced, or do not undergo the normal chan- 
ges, and remain ready, when the conditions shall become favorable 
in later life, from whatever reason, to commence growing with all 
the potencies of embryonic and lowly organized cells in the midst of 
the mature tissues. Not being restrained, however, by the regulat- 
ing influences which determine the nature and relative extent of 
growth in normal development, they go on to the production of tu- 
mors, which represent, though in atypical form, the various tissues 
which the strayed or unused cells were destined normally to pro- 
duce. 

The evident hereditary character of many tumors, the congenital 
nature and early development of others, their atypical structure in 
general, and the tendency of many forms to occur in situations in 
which, during the development of the embryo, considerable com- 
plexity exists, as well as their heterologous occurrence and their fre- 
quent primary multiplicity — all of these characters of tumors seem 
to favor Cohnheinr's hypothesis. On the other hand, the theory 
leaves unexplained the sudden growth of the alleged embryonal cells 
which have long remained dormant, and lacks as yet the absolute 
demonstration of a morphological basis, since no one has seen the 
strayed or delayed embryonic cells. These may, of course, be very 
small and difficult of demonstration, and this, according to Cohn- 
heim, fully explains the lack of a definite histological basis to his 
hypothesis. It should be remembered, furthermore, that, under or- 
dinary conditions in the body, certain cells which are destined to 
replace others which have fulfilled their destinies, as in the skin, pos- 
sess to a greater or less degree the characters of embryonal cells, 
and that while in the struggle for existence the growth of these cells 
may be held in check, as by conditions of pressure, nutritive supply, 
etc. , if these conditions be altered these cells may undergo prolifera- 
tive changes as significant as those of the alleged belated germs of 
Cohnheim. Such a changed condition of affairs has been shown by 
Thiersch to occur frequently in the skin in old age, and to explain 
in large measure the occurrence of certain epithelial tumors. 1 It 
should be remembered that this hypothesis was offered by Cohn- 
heim only as a suggestion to facilitate research, and that he ex- 
pressly warned his confreres against attaching a premature impor- 
tance to the possibility to which he called attention. Thus, while the 
hypothesis of the embrj^onal origin of tumors is most fascinating, 
and for certain forms quite satisfactory, we may well demand a 
more definite basis of fact before accepting it as of universal appli- 
cation. 

1 Consult Ribbert on the "Histogenesis of Carcinoma," Virchow's Archiv, 
Bd. cxxxv., p. 433, 1894. 



292 TUMORS. 

Bacteria have in recent times been claimed by some observers to 
stand in a causative relation to certain tumors, and bacteria have 
been occasionally demonstrated in, and cultivated from, the tissues 
of tumors. But no complete and reliable experiments or observa- 
tions have as yet been made which prove that they have anything tc 
do in causing the tumors, or are of any significance save as chance 
contaminations of the tissues or as inducing secondary complications. 

A great deal has recently been written — in view of the more 01 
less plausible notion that tumors might be of parasitic origin— about 
certain structures which are not infrequently found mostly in, bu1 
sometimes between, tumor cells, especially in the carcinomata, and 
which have been rather hastily assumed to be animal or vegetable 
parasites. These cell ' i inclusions " are for the most part larger 01 
smaller rounded bodies (Fig. 113); with or without nuclei; sometimes 
with double contours, sometimes not; usually sharply outlined against 







Fig. 113.— Epithelial Cell "Inclusions" in Tumors. 
Showing various forms. From carcinoma. 

the cell protoplasm in which they lie; often crowding the cell nucleus 
to one side, often situated within the nucleus, often apparently re- 
placing it. These structures seem to be invaginated epithelial or 
other cells, or cell nuclei which have undergone various degenerative 
metamorphoses, fragmentation, etc. In some vacuoles are developed : 
some lie in vacuoles in the tumor cells. They may be single or there 
may be several in a single tumor cell. Some of the questionable 
structures appear to be the metamorphosed nuclei of the tumor cells 
themselves. 

They are found in other than tumor tissues. 

These protean structures are no doubt of varied origin, and have 



TUMORS. 293 

been most frequently thought of late to belong among the cocci - 
dia. They are readily stained with varying degrees of intensity by 
hematoxylin, by eosin, by safranin, or by fuchsin. 1 Some of the cell 
inclusions in carcinoma may be coccidia or allied organisms. 

We do not, of course, assert that tumors cannot be caused by 
parasites, but at present it seems to us that no adequate ground 
exists for believing that they are. 

The nearly uniform failure of success in the transplantation of 
tumors from one species of animal to another, and the absolute failure 
to cultivate, either directly or by inoculation, any constant organisms 
from them, speak with much force against the notion of the parasitic 
origin of malignant tumors. 

It seems to the writer that to seek for a single external cause or 
group of causes for the aberrant tissue growths which we call tumors, 
is to ignore the many still obscure inherent influences which are at 
work in all tissue growth, especially those influences which, foster 
simple cell proliferation and tend, under the influence of heredity, to 
specialization in form or function. On the other hand, not to be 
ignored are those influences, whether of nutrition or pressure or ex- 
posure, which mould the cell growth under normal conditions into 
purposeful and fixed forms. 

It is rather a matter of surprise that ever-changing, self -regenerat- 
ing living tissue does not of tener go astray in its activities than that 
it only now and then should do so. This latter somewhat inverted 
point of view may be useful in calling away the attention, in dis- 
cussing the etiology of tumors, from a too close regard to extraneous 
factors, and directing it to the many still unexplored fields in cell 
physiology which we must perhaps become familiar with before we 
can, with fair hope of success, attack the problems, both in cause 
and cure, which crowd thickly about these significant tissue aberran- 
cies — the tumors. 3 

CLASSIFICATION OF TUMORS. 

The fact that tumors are composed of structures which resemble 
the various types of tissue found in the normal body suggests the 
guiding principle in their classification. But in order to thoroughly 
understand either the classification of normal tissues or the grouping 
of the tumors, we must keep in mind the way in which the tissues 
are developed in the embryo. 

According to the more recent views of embryologists, particularly 
of His and Waldeyer, the primitive tissues of the body belong to 
two groups: those of archiblastic and those of parablastic origin. 
In the early stages of foetal development the new cells which are 

1 Consult Stroebe, Centralb. f. allg. Path., etc., Bd. v., p. 110, 1894. 

2 See reference to asymmetrical karyokinesis in footnote, p. 93. 



294 TUMORS. 

formed at first arrange themselves in three layers, to which collec 
tively the name archiblast is applied. 

Of these three archiblastic layers, the outer, called the epiblas\ 
furnishes the material for the epithelium of the skin and its adnexs 
for the epithelium of the terminal portions of the alimentary cana 
and for the nervous system, including the neuroglia. 

The middle layer — the mesoblast — furnishes the material for th 
epithelium of the genito-urinary organs, and for both the smoot 
and striated muscle tissue. 

The inner layer — the hypoblast — affords the material for the dc 
velopment of the epithelium of the respiratory and the digestive sys 
terns, with that of the various glands and passages which develo 
out of and in connection with them. 

The exact origin of the parablast, which develops later than th 
archiblast, is still uncertain ; but it furnishes the material out c 
which are formed the connective tissues, including cartilage, bone 
teeth, and fat ; the blood cells and blood vessels ; the lymphatic tis 
sues and lymph vessels ; and the true endothelial cells. 

Now, if we wish to arrange in groups the different kinds of ti: 
mors found in the body, we have only to recall the varieties of tissu 
which normally exist there, and their grouping, and upon the class: 
fication of the physiological types to construct the classification c 
tumors. It should be remembered that the usual separation of th 
normal tissues into groups is useful, rather because it facilitates thei 
study than because it expresses absolute and fundamental distinc 
tions ; and the same may be said of all the classifications of tumors 
In both, an increase of our knowledge concerning their structur 
and genesis will doubtless lead to a more accurate grouping ; bui 
for the present, such an arrangement as that indicated below will b 
found of practical value for the purpose of studying tumors. 

I. Tumors composed of Tissues of the Type of those formin 
the Connective-Tissue Group. — 
Histioid or Connective-Tissue Tumors. 



Physiological Type. 


Tumors. 


1. Fibrillar connective tissue. 


1. Fibroma. 


2. Mucous tissue. 


2. Myxoma. 


3. Embryonal connective tissue. 


3. Sarcoma. 


4. Endothelial cells. 


4. Endothelioma. 


5. Fat tissue. 


5. Lipoma. 


6. __ Cartilage. 


6. Chondroma. 


7. Bone. 


7. Osteoma. 


8. Neuroglia. 1 


8. Glioma. 



1 It will be seen, from the account given above of the origin of the various tissue 
in the different embryonic layers, that the neuroglia has a different origin from th 



TUMORS. 295 

II. Tumors composed of Tissues of the Type of Muscle Tissue. 

— Myomata. 
Physiological Type. Tumors. 

1. Smooth muscle tissue. 1. Leiomyoma. 

2. Striated muscle tissue. 2. Rhabdomyoma. 

III. Tumors composed of Nerve Tissue. — Neuromata. 

Physiological Type. Tumors. 

1. Nerve tissue. 1. Neuroma. 

IV. Tumors composed of Vascular Tissue. — Angiomata. 

Physiological Type. Tumors. 

1. Blood vessels. 1. Angioma. 

2. Lymph vessels. 2. Lymphangioma. 

V. Tumors in which the Predominant or Characteristic Elements 
are Epithelial Cells. 

Physiological Type. Tumors. 

1. Glands. 1. Adenoma. , 

2. Various forms of epithelial cells 2. Carcinoma. 

and associated tissues. 

VI. . Tumors formed by Various Combinations of the above 
Types. — Mixed Tumors. 
Aside from the above well-marked classes, we may mention here 
for the sake of completeness : 

(a) Complex Congenital Tumors — Teratomata. — These are con- 
genital tumors which frequently contain a great number of different 
forms of tissue, such as various forms of fibrillar connective tissue, 
cartilage, bone, teeth, hair, skin, muscle, and glands. They are 
most frequently found at the lower end of the spine, about the head 
and neck, or in the generative organs. Some of them probably arise 
by an inclusion of portions of another foetus. These are called tera- 
toid tumors, or teratomata. Among them are sometimes classed 
other and simpler congenital formations, such as dermoid cysts, con- 
genital angiomata, and the so-called pigmented moles. 

(b) Cysts. — These structures, for the sake of convenience, are 
usually classed among the true tumors, although in general charac- 
ters, structure, and genesis they are of entirely different nature. 
They are usually divided into two classes : 

I. Cysts which develop in pre-existing cavities. 

II. Cysts which originate independently as the result of patho- 
logical changes. 

other connective tissues. The neuroglia, as well as the tumors derived from it, pre- 
sents marked peculiarities in structure, but its structural and functional alliance with 
the other connective tissues justifies its grouping among them. 



296 TUMORS. 

I. Cysts which develop in pre-existing cavities : 

1. Retention Cysts. — These are chiefly formed by the accumula- 
tion in glands or their excretory ducts of the mere or less altered 
secretion of the gland. They usually occur as the result of some 
hindrance to the normal discharge, as from inflammatory contrac- 
tions, pressure, etc. The contents of such cysts are usually mucous, 
sebaceous, serous, or of a mixed character. Their walls are the 
more or less altered walls of the original structure. To this class 
belong comedones, milium, atheroma, chalazion, ranula, the ovula 
Nabothi, milk cysts, and certain serous cysts of the ovaries, Fallo- 
pian tubes, gall ducts, and uriniferous tubules. 

2. Exudation Cysts. — These arise usually, though not always, 
as the result of a chronic inflammatory process in lymph spaces or 
serous sacs, and among them are to be classed the so-called gan- 
glia, hydrocele, etc. Certain of the so-called haematoceles, in which 
blood is extra vasated into closed cavities, form a variety of the cysts 
of this group. 

II. Cysts which originate independently as the result of patho- 
logical changes : 

1. Cysts formed by the softening and disintegration of tissue. 
— Such cysts may at first be small and have very meagre contents and 
no well-defined wall. A wall may finally be present either as an en- 
tirely new-formed structure, or the more or less modified capsule oi 
the organ in which they occur may partly or entirely form the wall. 
The contents of such cysts are usually the more or less altered de- 
tritus of the tissue by whose disintegration they are formed. Such 
cysts are very apt to occur within true tumors, particularly those 
which are succulent and of rapid growth, since these, as above 
stated, are very liable to degeneration. Old abscesses may change 
into well-defined cysts of this kind. 

2. Cysts formed around foreign bodies. — The inflammatory 
reaction induced by the presence of foreign bodies of various kinds, 
parasites, masses of extra vasated blood, etc., frequently results in the 
formation of well-defined encapsulated cysts. 

3. Cysts formed by a new growth of tissue in ivhose spaces 
various kinds of fluid accumulate. — These spaces may or may 
not be lined with epithelium and have something of the glandular 
character. Such forms are exemplified in some of the compound 
ovarian cysts — the so-called ovarian cystomata. 

4. Congenital Cysts. — These are of various forms, and their 
mode of origin is in most cases but imperfectly understood. The 
so-called dermoid cysts of the subcutaneous tissue and ovary are 
marked examples of this class. Certain congenital cysts of the kid- 
ney and other internal organs are conveniently grouped in this 



TUMORS. 29? 

class, although it is quite probable that some of them at least origi- 
nate during f cetal life in one or other of the above-described ways, 
and hence are not essentially different in nature from some of the 
cysts of other classes. For the mode of formation of certain cysts of 
the neck see page 538. 1 

Various Lesions sometimes described as Tumors. — There are 
certain enlargements of the lymph nodes which are in reality hyper- 
plasias, sometimes inflammatory in character and sometimes not, 
and which are often grouped among the tumors as lymphomata. 
They are not, strictly speaking, true tumors, and will be considered 
under the lesions of the lymph nodes. 

In the same group are often classed the enlargements of the 
lymph nodes in leukaemia and in other general diseases, which will 
be treated in another part of this book. Another group of tumors 
sometimes called lymphomata are in reality sarcomata, and these 
will be described under the latter heading. 

There is also a group of nodular new formations, the so-called In- 
fective Granulomata, which are sometimes classed among the tu- 
mors. These are found in tuberculosis, leprosy, syphilis, lupus, 
glanders, and actinomycosis. They seem, however, to be more 
closely allied to inflammatory new formations than to true tumors, 
and, as our knowledge regarding them increases, have one by one 
been proven to be dependent upon the irritation caused by the pre- 
sence of vegetable parasites (see section devoted to Infectious Dis- 
eases). In the case of syphilis the absolute proof is still lacking. 

Nomenclature of Complex Tumors. — The simple occurrence of 
more than one kind of tissue in a tumor does not make it a complex 
or mixed tumor. It is only when a special kind of tissue occurs in 
sufficient quantity to be of definite significance, or is of such a 
nature as to render its presence, in any amount, of importance, that 
we recognize its presence in the name. The name of mixed tumors 
is usually formed by joining the names of the tissues to be recog- 
nized. Thus a combination of fibroma and sarcoma is called fibro- 
sarcoma ; the general rule of construction being that the name of 
the more important tissue shall serve as the substantive which that 
of the less important one qualifies. It should be remembered, how- 
ever, that the more important tissue is not always the one which is 
present in greatest amount. Thus, owing to the great clinical sig- 
nificance of carcinomatous tissue, a very large fibroma with a small 
quantity of cancer tissue intermingled would be a fibro-carcinoma 
and not a carcino-fibroma. 

1 Consult for consideration of ciliated and other cysts, Hess, Ziegler's Beitr. zur 
path. Anat , Bd. viii. , p. 98, 1890; also Zahn, Virchow's Archiv, Bd. cxliii , p. 
170, 1896. 

24 






298 TUMORS. 

Preservation. — In general, tumors, like all tissues for microscopical study, should 
be cut into small pieces before immersing them in the preservative fluids, and the 
sooner they can be placed in these after removal the better will be the preserva- 
tion. In some cases much may be learned from large sections of tumors together 
with their surrounding tissues. In this case the proper part of the tumor must be 
preserved whole, and is best hardened in strong alcohol. 

It is often important in the study of tumors to examine not only the fully de- 
veloped or mature tumor structures, but also those portions in which the new growth 
is forming and in which it is encroaching on adjacent parts. 

So that in selecting portions of tumors for preservation and study, it is not wise 
to snip off a small piece at random, but a careful selection should be made, liberal 
portions being saved, from the centre, from the periphery, and from such surround- 
ing tissues as are available. For the ordinary routine hardening of tumors, Miiller's 
fluid followed by alcohol; strong alcohol: formalin, or sublimate may be recom- 
mended. 

For the methods of rapid preparation of sections for immediate diagnosis see 
p . 51. For studies on mitosis in tumor cells, sections may be made very thin by the 
method given on page 55, and stained with Heidenhain's hematoxylin. 



SECTION II. SPECIAL FORMS OF TUMORS. 

FIBROMA. 

The fibromata are composed of fibrillar connective tissue, which, 
as in the physiological type, is sometimes dense and firm, Fibroma 
durum, and sometimes loose in texture and soft, Fibroma molle. 
They are usually sharply circumscribed and are frequently encapsu- 
lated, but they may be diffuse and merge imperceptibly into the sur- 
rounding tissue. Some fibromata consist almost entirely of inter- 
cellular substance, containing but few flattened or spindle-shaped 
cells (Fig. 114) ; others contain very many variously shaped cells. 
The cells are often more abundant in one part of the tumor than in 




Fig. 114.— Dense Fibroma of Abdominal Wall— Fibroma durum. 
Some of the bands of connective-tissue fibres are cut across, others are cut lengthwise. 

another. The denser varieties usually contain but few blood vessels, 
although they are occasionally quite vascular. Many of the softer 
varieties are very vascular. Nerves also are occasionally seen. The 
course and arrangement of the fibres in these tumors are usually 
quite irregular, often crossing and interlacing in a most complex 
manner. The fibromata are usually of slow growth, but exception- 
ally they grow very rapidly. They are benign tumors, but by pres- 
sure on important organs, by ulceration, or by changing into other 
varieties of tissue, they may become of serious import. Pure fibro- 
mata do not form metastases, but they are often multiple, and when 
so are frequently' congenital. 

It seems probable that in the multiple fibromata of the skin (Fibro- 
ma molluscum) the new growths occur in some special form of 



300 TUMORS. 

connective tissue, as that of the nerves, blood vessels, or glands. 
Some of these multiple fibromata are classed among the neuromata* 

While the fibromata are more commonly nodular in form, when 
they develop on the skin or mucous membranes they frequently form 
papillary outgrowths covered more or less thickly with epithelium, 
and are then called papillomata (Fig. 115). Common warts of the 
skin are papillomata with excessive production of surface epithelium. 
To the papillomata also belong some of the so-called condylomata. 

Fibromata may, like most tumors, exhibit local recurrence when 
not fully removed. They are frequently very small and insignificant, 
but, on the other hand, may grow to an enormous size. 

They are quite frequently combined with other kinds of tissue to 
form complex tumors. The looser, softer varieties not infrequently 
become cedematous, when they may closely resemble myxomata. 
They are liable to calcification and to fatty and mucous degenera- 
tion. By metaplasia they may partially change to form fibro-chon- 
droma, fibro-lipoma, fibro-sarcoma, or fibro-osteoma. The latter 
transformation frequently occurs when they form in the periosteum. 
Developing, as they do, in the connective tissue, they occur in the 
most various parts of the body : in the skin and subcutaneous tissue ; 
in intermuscular tissue and fasciae ; in periosteum ; in the nerve 
sheaths and intraf ascicular connective tissue ; in the dura mater, the 
interstitial tissue of organs, and in the mucous membranes. Many 
of the so-called polypi of the mucous membranes (see Fig. 119) and 
some psammomata are forms of fibroma, the former often approach- 
ing the myxomata in type. 

Occasionally, in the ducts of glands, fibrous polypi grow to an 
enormous extent, their epithelial covering keeping pace in growth 
with their development, until they form very large, irregular, loose- 
textured tumors, which often finally ulcerate. Such forms are seen 
in the mammary gland, where they are frequently mistaken for car- 
cinomata. They are called Intracanalicular Fibromata (see Tu- 
mors of the Mamma). It is often difficult to distinguish between 
genuine fibromata and inflammatory or other connective- tissue hy- 
perplasias, such as elephantiasis ; and perhaps the fuller knowledge of 
the future will show that the distinctions are not as definite as we 
are now disposed to believe. 

MYXOMA. 

Mucous tissue is essentially an embryonic tissue, for in the normal 
adult it is present only in a very imperfect and atypical form in the 
vitreous of the eye, and perhaps exceptionally in small amount about 
the heart, kidneys, and medulla of bone. 

The myxomata are thus essentially embryonic-tissue tumors. 



TUMORS. 



301 



m 






mM* 




Fig. 115.— Small Papilloma of the Sklv. 
















r-^ 



tx 



\ " H« 

V f 



.fiSv i f / -^^' .__#*t j6- im k'J :. • i ij 



^—■^s 



Fig. 116.— Fibroma Molle from Subcutaneous Tissue. 
The stroma is cedematous, and in gross appearance the tumor resembled a myxoma 



302 TUMORS. 

These tumors consist, in their most typical forms, of a homogeneous 
or finely fibrillated, soft, gelatinous basement substance, in which are 
embedded a variable number of spheroidal, fusiform, branching, and 
often anastomosing cells (Fig. 117) . They may contain few or many 
blood-vessels and nerves. By the addition of acetic acid, mucin may 
be precipitated from the basement substance. In sections it is usu- 
ally stained with hematoxylin. The very soft forms which con- 







-:' 






'••"*% J >> . Pf ' . ) \ < > v -, f 1 









^;<i ' > f - A^4« '• f^ 







Fig, 117.— Myxoma of the Larynx. 
Showing the diffuse staining of the mucin-containing stroma with hematoxylin. 

tain comparatively few cells and much translucent basement sub- 
stance are called Myxoma gelatinosum or M. molle. The presence 
of many cells renders them more consistent and gives them a whiter 
and more opaque appearance ; such forms are called M. medullare. 
Pure myxomata are not very common. The myxomata are very 
apt to be combined with fibrillar connective tissue as fibro-myxoma ; 
or with fat tissue, lipo-myxoma ; and they very frequently become 
sarcomatous, or take part in the formation of very complex tumors. 
They may be diffuse or encapsulated with fibrillar connective tissue ; 
they are frequently very large, and may be multiple. Owing to the 
character of the basement substance, the blood, vessels not infrequent- 
ly rupture, giving rise to larger or smaller haemorrhages within the 



TUMORS. 



303 



tumor, or to the formation of cysts. The cells are liable to undergo 
fatty degeneration (Fig. 118). 

Composed, as they are, of a type of tissue from which fat tissue is 







Fig. 118.— Myxoma growing into Abdominal Cavity. 
Showing the accumulation of fat droplets in some of the cell bodies. 

developed in the embryo, the relations of these tumors to fat tissue 
are very intimate. They are most frequently developed in, and prob- 









Fig. 119.— Mucous Polyp of the Nose. 

The section shows the epithelial covering of the new growth, as well as its numerous blood 
vessels and a few mucous glands. 



ably directly from, fat tissue, and are very often combined with it 
as lipo-myxoma. They are also found in the subcutaneous, submu- 
cous, and subserous tissue, in the marrow and periosteum; in the 



304 TUMORS. 

brain and cord ; in the sheaths and intraf ascicular tissue of peripheral 
nerves ; in intermuscular septa ; and in the interstitial tissue ol 
glands, such as the mamma and parotid. The myxomata are ir 
general benign ; yet they are very prone, especially the lipomatous 
forms, to local recurrence. They sometimes grow very rapidly, anc 
sometimes, though very rarely, form metastases. In the not infre- 
quent combination with sarcoma they may exhibit the most markec 
malignancy. Many of the polypi of mucous membranes are myxo 
mata or fibro-myxomata (Fig. 119), and to this class of growths be 
long the so-called hydatid moles which sometimes develop in the vill 
of the chorion. 

([Edematous, loose, and cellular forms of fibrillar connective tissu( 
so closely resemble some of the forms of mucous tissue that certaii 
observers consider them as identical. So prone are many tumors t< 
undergo mucous degeneration, and so frequent are the combination! 
of the myxomata with other forms of tumors, that it is often dim 
cult, sometimes impossible, to say whether the mucous tissue in i 
given composite tumor is primary or secondary. 

SARCOMA. 

These tumors are formed on the type of connective tissue, bn 
they are, as a rule, largely composed of cells ; the basement sub 
stance, though a constant and important factor, being much less 
conspicuous than in adult connective tissue. They more closely re 
semble, in general, the developing connective tissue of the embryo oi 
the granulation tissue of inflammation. They are, therefore, con 
veniently described as presenting the type of embryonal tissue. Th( 
cells of the sarcomata are most varied in size and shape. They ma] 
be flat, fusiform, spheroidal, or branched, and even cuboidal or cylin 
drical; they may be multinuclear and very large, or they may b 
very small and spheroidal, resembling leucocytes. The fibrillar base 
ment substance may be present in such small quantity as to entireh 
escape a superficial observation, covered as it may be by the abnn 
dant cells ; or it may be so abundant as to give the tumor the genera 
appearance of a fibroma. It may be intimately intermingled witl 
the cells in fascicles, or it may be in large open-meshed networks 
giving to the tumor an alveolar appearance. The cells, however 
always stand in an intimate relationship to the basement substance 
which they sometimes reveal by fibrillar processes continuous witl 
it. Blood vessels also form a constant and important structural ele 
ment in these tumors, being in some of them so predominating r c 
factor that they give structural outline and general character to th< 
growth. They, too, as in the normal connective tissue, are intimate 
ly associated with the basement substance and with the tumor cells. 



TUMORS. 305 

A single form of cells is often so predominant as to furnish a suit- 
able qualifying name for the tumor, but in many cases the cell form 
varies greatly in the same growth. It may be said, in general, that 
there is a tendency to reproduce in these tumors some of the special 
characteristics of the tissues in which they originate. Thus, sarco- 
mata of the bones are apt to be osteo-sarcomata ; those of pigmented 
tissue, like the choroid, are apt to be pigmented sarcomata. It will be 
more convenient for our present purpose to briefly describe the more 
common forms one after another than to attempt any systematic 
classification of them. 

It should be remembered, however, that the various forms are 
not sharply specific in character, but are apt to merge into one another 
and to intermingle in various ways. 

Sarcomata are most frequently found in the skin, subcutaneous 
tissue, fasciae, subserous connective tissue, the marrow or periosteum, 
and in the choroid. They may also occur, though more rarely, in 
the dura mater ; brain and cord ; lymph nodes ; in the adventitia of 
blood vessels, and in nerve sheaths ; in submucous tissue ; in the ute- 
rus and ovary, and in the kidney. In the liver and lungs and heart 
they may occur by metastasis. 

They are more apt to occur at an early period in life than later. 
The cellular character, the rapid growth, the vascularity and succu- 
lence of many forms, the marked tendency to local recurrence, and 
the formation of metastases, stamp the sarcomata as malignant tu- 
mors. But in this they vary greatly ; while some of the forms be- 
long in every sense to the most malignant of tumors, others grow 
slowly, are very dense, and may remain localized and harmless for 
years. Their tendencies in this respect will be mentioned under the 
special forms. 

Intimately related as they are to the blood vessels, metastasis is 
more apt to occur through the blood than through the lymph chan- 
nels, and consequently adjacent lymph nodes are much less apt to 
be involved than in some other forms of tumor, notably the carcino- 
mata. 

The richly cellular and vascular forms of sarcoma are especially 
prone to haemorrhages, degeneration, and ulceration. 

Spindle-celled Sarcoma. — The cells in these tumors may be large 
— large spindle-celled S. (Fig. 120) ; or they may be small — small 
spindle-celled S. (Fig. 121) . They may consist largely of cells, or may 
contain so much intercellular fibrous tissue as to be appropriately 
called fibrosarcoma. The cells are frequently arranged in fascicles, 
which surround the blood vessels, and these fascicles may cross and 
interlace. These tumors, especially the small-celled forms, are, as a 
rule, denser and firmer and less malignant than other forms of sar- 
25 



306 



TUMORS. 



coma, but to this there are many exceptions. They may be encap- 
sulated or infiltrating. To this class belong the growths formerly 



-eft . -^ 




IS v 



Fig. 120.— Large Spindle-celled Sarcoma. 



F 



% 



■&■ 




W*~ 



Fig. 121.— Small Spindle-celled Sarcoma of Forearm. 



described as fibro-plastic tumors and recurrent fibroids. They fre- 
quently occur in the periosteum, subcutaneous tissue and muscle; 
in the uterus, and in various glands, notably in the mamma, tes- 



TUMORS. 307 

tide, thyroid, etc. These forms are among the most frequent of the 
sarcomata. 

Round-celled Sarcoma. — Of these there are two classes — 1, small 
round-celled sarcomata and, 2, large round-celled sarcomata. 

1. The small round-celled sarcomata consist of cells of about the 













Fig. 122.— Small Round-celled Sarcoma of Liver. 

size and appearance of mononuclear leucocytes (Fig. 122), and may 
have much or little intercellular substance, which may be irregularly 
disposed or arranged in large meshes resembling alveoli. In many 



fill 




! 






Fig. 123.— Large Round-celled Sarcoma op Leg. 

cases, so small is the quantity of intercellular substances that it is 
difficult of detection without special modes of preparation. These 
tumors are apt to contain many blood vessels, and be very soft and 
succulent. Their growth is sometimes rapid and they are often very 
malignant. 

They most frequently occur in the connective tissue of the mus- 



308 



TUMORS. 



cles and fasciae, in bone, and in lymph nodes {lymphosarcoma). 
They also occur in the internal organs, not infrequently in the brain, 
associated with glioma as glio-sarcoma (see page 386). 

2. In the large round-celled sarcomata (Fig. 123) the cells vary in 
size, but are usually very much larger than in the last variety. Their 
nuclei are usually large and contain prominent nucleoli. They, too, 
are often very vascular, and contain a variable quantity of basement 
substance. They are occasionally alveolar in character. They are, 
as a rule, less soft and malignant than the small-celled varieties. 

The round-celled sarcomata were formerly supposed, on account 
of their macroscopical and clinical resemblance to some of the soft 
forms of carcinoma, to belong to these tumors, and were called me- 
dullary cancers. 




Fig. 124.— Melano-Sarcoma from Submaxillary Region. 



Melano-Sarcoma. — These tumors consist most frequently of spin- 
dle cells of various sizes, although cells of other shapes frequently 
occur in them. They are characterized by the presence in the cells, 
and less frequently in the intercellular substance, of larger and 
smaller particles of brown or black pigment (Fig. 124). The pigment 
is usually quite irregularly distributed in patches or streaks, and is 
located chiefly in the cell body. They arise most frequently in the 
skin and in the choroid. Pigmented moles of the skin often form 
their starting points. They belong to the most malignant of tumors. 
They very readily form metastatic tumors in various parts of the 
body, which are, like the parent tumor, pigmented. 

Various forms of tumors may contain brownish pigment deposited 
in them by the degeneration of the haemoglobin from extra vasated 
blood; these should not be mistaken for melanotic sarcomata. 1 

Myeloid or Giant-celled Sarcoma. — Tumors of this class are 
usually formed chiefly of spheroidal or fusiform cells of variable size, 

1 On the occurrence of melanuria in cases of melano-sarcoma consult Thacher, 
Transactions New York Pathological Society, 1893, p. 105. 



TUMORS. 



309 



but their characteristic feature is the presence of larger and smaller 
multinu clear cells, called giant cells (see foot note on page 218). 
These are closely intermingled with the other cells, and may be very 
abundant or very few in number (Fig. 125). Giant cells may occa- 
sionally occur in other tumors, but are most abundant and charac- 
teristic in these. These tumors are chiefly formed in connection with 
bone, and may commence in the marrow or in the periosteum. They 
are sometimes very soft and vascular, and subject to interstitial 
haemorrhages. Some of these vascular sarcomata were formerly 
classed together with other kinds of vascular tumors as fungus nema- 
todes. Some of the forms of epulis are giant-celled sarcomata. 



fSu 



NiBfe£ 





. 




Fig. 125.— Giant celled Sarcoma of Bone. 



When these tumors originate in the marrow of the long bones, 
which is a favorite place for them, they are apt to cause resorption 
of the bone ; and although the tumor may be for a long time enclosed 
by a shell of new-formed bone, which enlarges with the enlarging 
tumor, it usually, sooner or later, breaks through this and infiltrates 
adjacent tissues. They are liable to form metastases and frequently 
grow to a very great size. The periosteal forms are apt to be firmer 
in texture, and are prone to the development of irregular masses of 
new bone within them, thus forming one of the varieties of osteo- 
sarcoma, 

Osteo-Sarcoma. — These are spindle or round-celled tumors, usu- 
ally, but not always, connected with bone, in which irregular masses 
of bone tissue are present. The bone is usually of irregular atypical 



810 



TUMORS. 



structure, the regular lamellation and typical Haversian cana! 
being usually absent. They may form metastases which presei 
similar characters. 

Calcification, which should be distinguished from ossificatioi 
may occur in various forms of sarcoma. 

Anglo-Sarcoma. — In many of the sarcomata in various parts c 
the body the blood vessels form so prominent and important a fe£ 
ture as to give special character to the growth, not alone by thei 
size and general prominence, but sometimes by the peculiar arrangt 
ment which their presence gives to the cells. While in most of th 
sarcomata the blood vessels have a very important influence in detei 
mining the topography of the tumor, in most of the denser and i 







Fig. 126.— Angio- Sarcoma of Liver. 
The thin-walled blood vessels, around which the tumor cells are formed, are irregularly dilated. 



many of the softer varieties this influence is not easily traced. I 
many forms, however, particularly those which are soft and ver 
cellular, the cells are closely grouped around the vessels, as if the 
were developed in their adventitise and had formed close sheath 
around them. The masses of cells thus formed, with a blood vess( 
for a centre, may be closely packed together in long strings wit 
more or less frequent anastomoses (Fig. 126), or they may be ai 
ranged in rounded groups, giving to the tumor an alveolar appeal 
ance. Such tumors are called angio-sarcomata. Simple vascu 
larity, although this be extreme, does not make of a tumor an angic 
sarcoma. 



TUMORS. 



311 



Alveolar Sarcoma. — Sometimes, as above stated, the basement 
substance of the sarcomata, particularly in some of the round-celled 
varieties, is quite abundant and arranged in a wide-meshed net, in 
the meshes of which the cells lie. These spaces are called alveoli, 
and this variety of structure has acquired importance from the gene- 
ral resemblance which these tumors have to the well-defined and 
characteristic alveolar structure which many of the carcinomata ex- 
hibit. It is true that occasionally the resemblance is very close 
indeed, but usually the sarcomata present a more or less intimate 




MSErTr 

Fig. 127.— Myxosarcoma of Pharynx. 



relation between the cells and basement substance. The cells usually 
do not simply lie in the cavities, but are often attached to the inter- 
cellular substance, which not seldom sends finer trabeculae into the 
alveoli between the cells. Sometimes a careful shaking of sections 
in water is necessary to reveal the characters of the reticulum. The 
cells, moreover, are usually, though not always, distinctive in cha- 
racter. This form of tumor is, in some cases at least, determined, as 
above stated, by the new formation and peculiar arrangement of the 
blood vessels. Tumors of this kind are not common, but may occur 
in the skin, lymph nodes, bones, and pia mater. They are usually 
very malignant. 

Mixed Forms of Sarcoma. — In addition to the above more or 
less well-defined forms of sarcoma, there exist various modifications 
which have received special names. The sarcomata in which cysts 
form, either by the softening of tissue by degeneration, or by the 
dilatation of gland ducts by pressure, or by the new formation of 



312 



TUMORS. 



tissue in gland ducts or alveoli which dilate with the growth of the 
tumor, have received the name of cysto-sarcomata. 

Mucous degeneration is frequent in the various forms of sarcoma. 
A combination of myxoma and sarcoma — myxo-sarcoma — is com- 
mon (see Fig. 127). 

Combinations of sarcoma with fat tissue, lipo-sarcoma ; with 
glandular structures, adeno-sarcoma (Fig. 128); with cartilage, 
chondrosarcoma ; with muscle tissue, myosarcoma ; and with va- 
rious other tissues, are of frequent occurrence. Some forms of psam- 
moma, or " brain sand," found chiefly in the dura mater, are fibro- 












Fig. 128.— Adeno-Sarcoma of Parotid. 



sarcomata which have undergone calcification, the lime being de- 
posited in lamellated masses of various shapes within them. 

Some of the soft papillomata and warts, and occasionally the 
polypi of the mucous membranes, belong to the type of sarcoma or 
myxo-sarcoma. 

The so-called chloromata, which have been found in a variety of 
places in the body, but are rare, are apparently forms of sarcoma. 
Chloroma is characterized by a greenish color, ^ he nature of which is 
not known. 1 

ENDOTHELIOMA (ENDOTHELIAL SARCOMA). 

Under the name endothelial sarcomata or endotheliomata are 
grouped a number of tumors which on the one hand are closely related 

1 For a review of literature of chloroma see Lang, Arch. gen. de Med., 1893, vol. 
ii., p. 555: 1894, vol. i., pp. 63, 186, 313. For the relationship of chloroma to 
leukaemia see Dock, American Journal of the Medical Sciences, August, 1893. 



TUMORS. 



313 



to the sarcomata in genesis, and in some cases in appearance, while 
on the other hand some of them so closely resemble some forms of 




Fig. 129.— Endothelioma of Upper Jaw. 
Showing dense connective tissue surrounding the blood vessels between the reticular endo- 
thelial cell masses. 




Fig. 130.— Endothelioma (Endothelial Sarcoma) op Dura Mater. 



carcinoma as to be difficult of distinction from them. The endothe- 
liomata originate in that form of connective-tissue cells called endo- 
thelium, lining lymph vessels or lymph spaces, and develop by a 

26 



314 TUMORS. 

proliferation of these cells. Sometimes the cells of the endothelic 
mata resemble closely the normal endothelium; sometimes, howevei 
they differ considerably from them, being occasionally very larg< 
often thick and irregular in shape, and even nearly cylindrical c 
cuboidal like certain forms of epithelium. They are associated wit 
a more or less abundant vascular stroma, which may be alveolar i 



?m 



Ms -b, 






/,::.v> 






^v-p,^-^ ^ ^ ^ .'.--■"> z ^*'f 









■'oo, %Q>°° o ^% S 

fc? ^° ^ :> : ; • l ; * *> 3 ^r : ' • ■■■■ "'- ~~ ^-^-S>te^ 



i S r ':3^S 



.Q .. O = ^W,- 


















£J 



Fig. 131.— Endothelioma of Pleura. 



Showing the formation of mucus within the endothelial cell masses; the mucus is stain' 
with hsematoxin. 



formation. In this case, as in alveolar sarcoma, it may often be see 
that the cells have an intimate relationship to the trabecule of tr 
stroma. 

Developing from the endothelium of the lymph vessels, the* 
tumors sometimes exhibit a structure closely simulating that < 



TUMORS. 



315 



tubular glands lined with more or less cuboidal epithelium. It is in 
many cases difficult to decide from the structure in the fully developed 
parts of tumor whether it is an endothelioma or a carcinoma. In 
such cases a careful study of the peripheral portions of the tumor 
and parts into which it is extending may reveal early phases of pro- 
liferation in the endothelium of lymph vessels or spaces (Fig. 129). 
In this case its genetic relationship will determine the nature of the 
tumor, however similar it may be in morphology to carcinoma. 

Sometimes the cells of the endotheliomata are packed together in 
dense concentric masses (Fig. 130), which may have a glistening ap- 




Fig. 132.— Endothelioma op Upper Jaw. 

Showing formation of mucus in the gland-like endothelial cell masses. This form of tumor is 
often called " cylindroma." 



pearance, and such tumors are sometimes called cholesteatomata. 
Although, for the most part, the peculiar glistening appearance of 
these tumors is due to the closely packed thin cells which compose 
them, they not infrequently contain crystals of cholestearin, which 
may share in producing this characteristic appearance. But the 
cholestearin may be absent, or present in small amount. 

The stroma of the endotheliomata may undergo various forms of 
alteration, developing hyalin, myxomatous, or cartilaginous or very 
dense fibrous characters (Fig. 129) ; or it may atrophy, leaving the 
proliferated endothelium and the blood vessels as the chief structural 



316 



TUMORS. 



elements. On the other hand, hyalin and mucous degeneration of 
the endothelial cells may occur (Fig. 131), and considerable collec- 
tions of these materials, free from the cells but surrounded by the 
cell masses, may give a cystic character or lend a glandular appear- 
ance to the growth (Figs. 132, 133). 

Such tumors — in which homogeneous or striated cylinders of 
hyalin or mucoid material, often closely surrounded by layers of 
cuboidal or flattened cells, form a striking feature — have sometimes 
been called cylindromata. The stroma of the endothelioma may be- 




Fig. 133.— Cylindroma (Adenoma) of Antrum. 

This complex form of cylindroma, resembling types of adenoma, not infrequently occurs in 
the ovary. 

come sarcomatous and thus a mixed tumor — a sarcomatous endothe- 
lioma — may be formed. 

The endotheliomata may be single, nodular, and of considerable 
size ; or they may be multiple, numerous small tumors being scattered 
over the surface of the part in which they grow. They may even 
form a thick or thin pellicle over surfaces, or cause adhesions between 
adjacent organs. They may form metastases. They occur in the 
dura mater and pia mater, in the pleura and peritoneum, and have 
been described in the skin, boue, gums, lymph nodes, ovary, liver, 
brain, testicle, glandula carotica, and salivary glands. 1 



"' For an admirable study of the endotheliomata with bibliography consult Tolk- 
mann, Deutsche Zeitschr. f. Chirurgie, Bd. xli., p. 1. 



TUMORS. 317 



LIPOMA. 



Lipomata are tumors formed of fat tissue. The fat tissue occurs in 
lobules and is similar to normal fat, except that the cells and lobules 
are usually larger and less regularly arranged. There may be little 
connective tissue in the tumors, when they are very soft, almost fluc- 
tuating — lipoma molle — or there may be so much as to give the 
tumor considerable firmness— ftbro-lipoma. They may be in part 
transformed into mucous tissue — myxo-lipoma. Cartilage not infre- 
quently develops in them, or they may undergo partial calcification. 

Occasionally the blood vessels are very abundant and dilated — 
angio-lipoma. They are usually sharply circumscribed, but may 
infiltrate surrounding tissues. They are not infrequently pedicu- 
lated. They sometimes grow to enormous size and may ulcerate. 

They are usually isolated, but may be multiple. They are the 
most common of tumors, occurring usually in the subcutaneous or 
other fat tissue. They may occur in the mucous membrane of the 
gastro-intestinal canal, in the peritoneum, more rarely in the dura 
mater, kidney, liver, and lungs. They are benign tumors, not form- 
ing metastases ; but they may be deleterious by ulceration or gan- 
grene, and when not fully removed may exhibit local recurrence. 

CHONDROMA. 

These tumors, composed of either of the physiological forms of 
cartilage, are usually hard, but sometimes quite soft. The cells do 
not present the same uniformity in size, shape, number, and relative 
position that they do in normal cartilage. Sometimes they are very 
large, spheroidal, and grouped in masses, and again small and far 
apart. They are frequently fusiform or branching. Fibrillar con- 
nective tissue in varying quantity is usually present in the chondro- 
mata, either as a capsule, or running in bands between the nodules 
of - cartilage, or passing in fascicles into them (Fig. 134). The carti- 
lage may change to mucous tissue, forming myxo-chondroma 1 (Fig. 
135) ; the cells may undergo fatty degeneration or they may calcify 
or ossify. Chondromata frequently form a part of mixed and com- 
plex tumors. 

They may form in connection with bone or cartilage, and are 
often traceable to irregularities in foetal development. Or they may 



1 This change of. one form of tissue into another is called metaplasia (see page 
95), and is not uncommon among tumors formed on the connective-tissue type. 



318 



TUMORS. 



occur in soft parts where cartilage is not normally present, as in the 
parotid, testicle, mamma, and ovaries, where they are apt to be 



tfRfc*iafflfo 



_jm^wmm§^ 






'Ji'j'-U^''' 



fJMiffiVw, 



Fig. 134.— Chondroma of Subcutaneous Connective Tissue. 




mixed with other tissue; or in subcutaneous connective tissue and 
fascise. 




Fig. 135.— Myxo-Chondroma of Cervical Region. 



They are in general benign tumors, but metastases sometimes oc- 
cur, most frequently in the lungs, sometimes in the heart. 

Small hyperplastic growths on the surfaces of cartilage are called 
ecchondroses. 



TUMORS. 319 



OSTEOMA. 



The formation of bone in the body in abnormal places occurs 
quite frequently and under a great variety of conditions. It is on 
this account not easy to define the term osteoma, and it is frequently 
difficult to determine whether or not a given mass of new-formed 
bone is an osteoma or not. Bone tissue often occurs in tumors of 
the connective-tissue group as a secondary or complicating struc- 
ture — osteo-fibroma, osteo-chondroma, osteosarcoma, etc. It may 
occur in muscles as a result of certain exercises, or as a result 
of a peculiar inflammatory process (see Lesions of the Muscles), or 
it may occur in connection with chronic inflammation in a variety 
of tissues. A circumscribed mass of abnormal bone, not of inflam- 
matory origin, may be called an osteoma. Small masses of new- 
formed bone of various shape, projecting from a bony surface and 
frequently of inflammatory origin, are usually called osteophytes. 
Bony tumors projecting from the surface of bones are frequently 
called exostoses. 

An osteoma may be loose in texture, consisting of bone tissue 
similar to cancellous tissue ; or it may be denser, resembling compact 
bone tissue ; or it may be very hard and dense like ivory, so-called 
ivory exostoses. The difference between these forms lies chiefly in 
the varying number and size of the vascular and medullary spaces 
which they contain. 

Osteomata may develop in connection with the bone or peri- 
osteum, which is most frequently the case, or, independently of bone, 
in soft parts. 

New-formed bone has been found in the soft parts of the body, in 
the brain substance, dura mater, and pia mater ; in the pleura, 
diaphragm, and pericardium ; in the skin, choroid, air passages, 
lungs, and penis, and in other places. To what extent some of these 
bone formations may have been due to inflammatory action it is 
not possible to say, and it is quite probable that the fuller knowl- 
edge of the future may show relationships between the development 
of certain tumors and some forms of chronic inflammation which we 
do not now recognize. 

The growth of the osteomata is, as a rule, slow. They are benign 
tumors, and are not infrequently multiple. 

ODONTOMA. 

Tumors are sometimes formed from the pulp during the develop- 
ment of the teeth. When these contain dentin they are called 
odontomata. 



320 



TUMORS. 



GLIOMA. 

Th3 gliomata are developed in connection with the characteristic 
connective-tissue framework of nerve tissue, the neuroglia, which ii 
structure many, though usually not all, of its cells closely resemble 
Small cells with inconspicuous bodies and numerous delicate branch 
ing processes are most characteristic ; but in connection with thes< 







Fig. 136.— Glioma of Brain. 



there is usually a greater or less number of small spheroidal cell 
with proportionally large nuclei (Fig. 136). It is usually necessar; 
to shake sections in water or carefully tease fragments of the tumo 




Fig. 137.— Neuroglia or " Spider " Cells from Glioma of Brain. 
Teased specimen. 

in order to see the characteristic neuroglia or so-called " spider" cell 
( Fig. 137). These tumors may contain very numerous and frequently 
dilated thin- walled blood vessels. They may be very soft or mode 
rately hard ; and, especially when occurring in the substance of th 
brain, are frequently not sharply outlined against the adjacent nor 
mal tissue. They usually occur singly, and are comparatively slov 
in growth. 



TUMORS. 321 

They are very apt to be complicated with other tumor tissue, 
forming glio-myxoma, gtio-sarcoma, etc. Owing to the abun- 
dance of thin- walled blood vessels and the softness of the growth, 
they are liable to interstitial haemorrhages, and may then, when oc- 
curring in the brain, readily be mistaken for ordinary apoplectic 
clots. They are liable to fatty degeneration. They usually occur in 
the brain, spinal cord, and in the optic and other cerebral nerves. 
The so-called gliomata of the retina are usually small spheroidal- 
celled sarcomata. 

Pure gliomata are benign tumors, though in their most common 
combination with sarcoma they may be very malignant. Their usual 
situation, however, is such as to make them almost always signifi- 
cant, although technically they are benign tumors. 1 

MYOMA. 

Tumors composed of muscular tissue are of two kinds, following 
the two physiological types of muscle tissue, the non-striated and the 
striated. 




lite 

— <^ — 

Fig. 138.— Myoma op Uterus— Leiomyoma. 

I. Leiomyoma, Myoma levicellulare. — The characteristic ele- 
ments of these tumors are fusiform, smooth muscle fibres, with 
elongated or rod-shaped nuclei. These are packed closely together, 
frequently interlacing and running in various directions, and are in- 
termingled with a variable quantity of more or less vascular fibrillar 
connective tissue (Fig. 138). When, as is not infrequently the case, 
the connective- tissue elements are present in large amount, the tumor 
is called fibro-myoma. It is not always easy in sections to distinguish 
between these tumors and certain cellular fibromata, but the cha- 
racteristic shape of the isolated cells and their nuclei, together with 

1 Our knowledge of the normal neuroglia is still too meagre to permit us to under- 
stand very thoroughly this class of tumors, and to separate it as precisely as could be 
wished from certain of its allies among the abnormal connective-tissue growths. 
27 



322 TUMORS. 

their uniformity in size, will usually suffice. These tumors are fre- 
quently infiltrated with lime salts, and, owing to their density and 
lack of blood vessels, they not infrequently degenerate, forming cysts 
or becoming gangrenous. They may occur singly or be multiple, 
are usually of slow growth, may be large or small, and are benign. 
They may occur wherever smooth muscle tissue exists. They are 
most frequently found in the uterus, where they are often multiple, 
They may occur in the wall of the gastro-intestinal canal, and have 
been seen in the bladder and in the skin. The so-called hypertrophies 
of the prostate, so frequent in advanced life, are sometimes con- 
sidered leiomyomata of the interstitial muscle tissue of that gland. 

II. Myoma striocellulare, or Rhabdomyoma. — In these rare tu 
mors striated muscle fibres are the characteristic elements. The} 
very rarely compose a great part of the tumor, but are interminglec 
with other elements, fibrillar connective tissue, spindle-shaped anc 
spheroidal cells of various forms, which often appear to be incompletely 
developed muscle cells. They are not infrequently associated with sar 
comatous tissue. Blood vessels and sometimes nerves are also present 
The muscle fibres differ, as a rule, from normal striated muscle fibre 
in their arrangement, which is usually quite irregular, and also ii 
size, being in general smaller than normal fibres, although varying 
greatly. The sarcolemma is either absent or incompletely developed 
These tumors are usually small or of moderate size, and are suppose< 
to originate from inclusions of cells destined to form muscle tissue ii 
places where they do not belong. 

In the heart and certain other muscular parts small circumscribe< 
^masses of striated muscle tissue have been described, and are some 
times called homologous rhabdomyomata. But genuine heterolc 
gous rhabdomyomata are, in almost all cases thus far recorded 
confined to the genito-urinary organs, kidney, ovary, and testicles 
The writer has described an exceptional case of rhabdomyoma occui 
ring in the parotid gland. 1 

These tumors, when not associated with other and malignan 
tumors, are benign and are of much greater theoretical than practica 
interest. 

NEUROMA. 

A true neuroma is a tumor containing new-formed nerve tissue 
Such tumors are comparatively rare. Tumors developed in the con 
nective tissue of nerves and composed usually of fibrous or mucou 
tissue are common, and are frequently called neuromata, but the; 
should be called fibromata or myomata, etc., of the nerves, or fals 

1 American Journal of the Medical Sciences, April, 1883. For literature an 
bibliography consult Ribbert, Virchow's Archiv, Bd. cxxx., p. 249. 



TUMORS. 



323 



neuromata. The true neuromata are of two kinds, ganglionic or 
cellular neuromata and fibrillar neuromata, depending upon the 
character of nerve tissue which they contain. The ganglionic neu- 
romata — neuroma ganglioniforme — in which new-formed nerve cells 
are present (Fig. 139), are found associated with other structures in 
certain of the teratomata in the ovaries, testicles, and in the sacral 
region ; they also occur in the gray matter of the brain. They have 
been found in the suprarenal glands. 

The fibrillar neuromata are, according to Virchow, of two kinds, 
myelinic and amyelinic % depending upon whether the nerve fibres 
which they contain are medullated or not. The neuroma myelini- 
cum is the more common and the best understood. The medullated 
nerve fibres in these tumors are associated with fibrillar connective 
tissue, and are usually curled and intertwined in a most intricate 
manner. They occur either singly or multiple on the peripheral 




Fig. 139.— Neuroma ganglioniforme. 
From the suprarenal gland. 



nerves. They may occur in considerable numbers as nodular tumors 
on the branches of a single nerve trunk, or they may form an irregu- 
lar, diffuse, nodulated enlargement of the nerve branches— plexiform 
neuroma. These neuromata may or may not be painful. They not 
infrequently form at the cut ends of the nerves in amputation stumps. 
They are benign tumors, never forming metastases. 

The false neuromata (Fig. 140) are myxomata, or fibromata, or 
sometimes myxo-sarcomata of the nerve sheaths or intraf ascicular 
connective tissue, and may occur singly or multiple. In the latter 
case they may affect the branches of a single nerve trunk, or they 
may be found on nearly all the cerebro-spinal peripheral nerves. 
The writer has described a case (Figs. 141 and 142, pages 324 and 325), 
in which over eleven hundred and eighty-two distinct tumors were- 
found distributed over nearly all the peripheral nerves of the body. 1 

1 American Journal of the Medical Sciences, July, 1880. 



324 



TUMORS. 



The nerve fibres in these tumors may be crowded apart by the 
new growth and considerably atrophied ; or, in cases in which the 




Fig. 140.— Fibroma (False Neuroma) of Lumbar Nerve. 
The fibrous tissue is loose in texture and in places cedematous, so that it considerably re- 
sembles mucous tissue. 

tumor is composed of soft tissue, as in myxoma or the soft fibro- 
ma, they may pass through or around the tumor entirely un- 
changed. The multiple false neuromata are in many cases con- 
genital. 




Fig. 141.— Multiple Fibromata (False Neuromata) of Pneumogastric Nerve. One-quarter 
natural size. 



ANGIOMA. 



Angiomata are tumors consisting in large part or entirely of new- 
formed blood or lymph vessels or cavities. In many tumors of vari- 
ous kinds the new-formed or the old blood and lymph vessels may be 



TUMORS. 



325 




Fig. 142.— Multiple Neuromata of the Peripheral Nerves. 

A, Nerves of the right arm; B. the left sciatic with its branches; C. the left anterior crural 
with its branches. 



326 TUMORS. 

very abundant or prominent by reason of their dilatations ; the ves- 
sels of otherwise normal tissues may also be largely dilated, thus 
simulating vascular tumors. These are, however, not true angio- 
mata, although sometimes reckoned among them, and in many cases 
closely allied to them. Such are the so-called arterial varix, or ci p- 
soid aneurisms, and haemorrhoids, and various lymphectasiae. True 
angiomata are of two kinds — I., Hcemangioma, and II., Lymph- 
angioma. 

I. Hcemangiomata. — These tumors are of two types : 1. Those 
formed largely of capillary blood vessels with either thin or thickened 
walls, embedded in a more or less abundant connective-tissue stroma. 
These are called simple angiomata or angioma telangiectoides. The 
walls of the vessels in these tumors are frequently dilated or pouched, 




Fig. 143.— Angioma telangiectoides (Vascular Naevus). 
From skin over scapula of child. 

and usually form a tangle of curled and intertwined vessels (Fig. 143). 
They occur most frequently in the skin or subcutaneous tissues, 
usually about the face, and may project above the general surface 
or be on a level with it. Such are the so-called vascular nmvi, or 
strawberry marks, which are usually congenital. They are some- 
times sharply circumscribed, and sometimes merge imperceptibly 
into the surrounding skin. They sometimes occur in the mucous 
membranes, in the mamma, bones, and brain. They are benign 
tumors, never forming metastases, but may be associated with sar- 
comata. 

2. The second form of hemangioma, called angioma cavernosum, 
consists largely of a series of intercommunicating, irregular-shaped 
larger and smaller blood spaces lined with endothelium, and sur- 
rounded by a variable quantity of fibrillar connective tissue, which 



TUMORS. 



32? 



may contain smooth muscle cells (Fig. 144). They resemble the erec- 
tile tissue of the corpora cavernosa of the penis and clitoris. They 
are apparently formed by a dilatation of old and new-formed capil- 
laries and veins. They are sometimes erectile and sometimes pulsat- 
ing, and are not infrequently multiple. They may be seated in the 



'LT 



ST 




Fig. 144.— Angioma cavebnosum of Liver. 



skin and subcutaneous tissue, forming the so-called projecting naevi, 
or in internal organs. They are often found in the liver and less 
frequently in bone, the brain, spleen, uterus, kidney, intestines, blad- 




Fig. 145.— Congenital Lymphangioma prom Arm of Child. 

der, and muscles. They are usually of little significance, though 
they may give rise to haemorrhages. 

II. Lymphangioma. — These tumors consist of dilated lymph 
channels, which either preserve approximately the general shape of 
the original lymph vessels, or are distinctly cavernous in character, 
or even cystic (Fig. 145). They probably originate in part in new- 



328 TUMORS. 

formed, in part in old lymph channels. A strict distinction betweer 
tumors formed by a dilatation of preformed and new-formed lymph 
channels is not possible, owing to the very primitive character of some 
of the ultimate lymph spaces and our lack of knowledge of their exad 
relations to adjacent parts. 

In the lymphangiomata there may be much t or little connective 
tissue between the dilated channels, which are usually filled with a 
translucent or milky fluid resembling, and probably identical with, 
the normal lymph. These tumors are usually congenital, but are 
sometimes acquired. They usually occur in the skin as soft, some- 
times considerably, sometimes but slightly elevated tumors, and may 
occur in the tongue — some forms of so-called macroglossia. They 
are benign tumors, but may rupture, giving rise to a serious lymph- 
orrhcea. 

TUMORS IN WHICH EPITHELIAL CELLS ARE PREDOMINANT OR 
CHARACTERISTIC ELEMENTS— EPITHELIAL TUMORS. 

I. Adenoma. 

II. Carcinoma. 

General Considerations. — The tumors thus far described in de- 
tail, with the exception of the gliomata, are formed on the type of 
tissues which develop from the parablast. The epithelial tumors, on 
the other hand, originate in one or other of the layers of the archi- 
blast, and we have accordingly two series of criteria by which to de- 
scribe and identify them : first, morphological, and second, histoge- 
netic criteria. 

While in the main, in the normal body, the general distinctions 
between epithelial and other tissues are fairly well marked, there are 
still particular cases, especially those in which epithelial tissues are in 
process of physiological growth or rejuvenation, in which the dis- 
tinctions are quite ill-defined. When we remember the rapid growth 
of many tumors, the tendency to incomplete formation of their cells, 
their diverse seats, and the various complicating conditions under 
which they originate and develop, it does not seem strange that the 
exact limitations of this class of tumors are not easy to fix, nor that 
they seem sometimes to merge into one another and into tumor tis- 
sues belonging to other classes. If epithelial cells, under all circum- 
stances, had a definite and characteristic structure, or if, on the other 
hand, we could always know whether a given cell group originated 
in epithelium or not, the matter of distinguishing between tumors of 
this and other classes would be simple and easy enough. As it is, in 
some cases both morphological and histogenetic criteria fail us, and 
the clinical history and gross appearance are not characteristic. Such 
cases — which are indeed rare, but which do sometimes occur — suggest 



TUMORS. 329 

to us the possibility that the desirability of accurate classification has 
led us into seeking distinctions which Nature herself has not sharply 
drawn. While these difficulties in special cases must be acknowl- 
edged, tha distinctions are in the main definite enough, and very use- 
ful both for clinical and scientific purposes. 

Epithelial tumors always contain, in addition to the more or less 
characteristic cellular elements, a connective-tissue stroma which 
gives them support and carries the vessels. This stroma may be 
sparse or abundant, may contain few or many cells, is sometimes ar- 
ranged in irregular fascicles or bands, and very frequently forms the 
walls of well-defined, variously-shaped spaces or cavities called alve- 
oli, in which the epithelial cells lie. The epithelial cells, in most 
cases, lie along the walls of the alveoli without an intimate connec- 
tion with them, as is the case in the alveolar sarcomata. They are, 
moreover, packed together without more intercellular substance than 
the usual cementing material common to epithelial cell masses. In 
this lack of fibrillar intercellular substance within the alveoli, and in 
the loose relationship between the cells and the alveolar walls, lie in 
many cases the chief morphological distinctions between certain car- 
cinomata and alveolar sarcomata. 

In certain of the epithelial tumors there is a reproduction of typi- 
cal gland tissue of various kinds, depending upon the seat and condi- 
tions of growth of the tumor. Such tumors are called adenomata. 
A simple hypertrophy of a gland, or an increase in its size by exces- 
sive growth of its interstitial tissue, does not constitute an adenoma. 
There must be an actual new formation of more or less typical gland 
tissue. This is not always or frequently of exactly the same charac- 
ter as the gland tissue in which it originates, and always exhibits a 
certain lack of conformity to the type in structure and mode of 
growth. The alveoli and ducts usually have a lumen and some- 
times a membrana propria, but the cells may differ in shape from one 
another and from those of the gland from which they spring. 

Epithelial tumors in which there is no close conformity to a glan- 
dular type, but a lawless growth of various kinds of more or less 
typical epithelial cells in the meshes of an old or new-formed connec- 
tive-tissue stroma, are called carcinomata. 

It will readily be seen that there must be a border region between 
the adenomata and carcinomata, where conformity to the glandular 
type merges into the lawlessness of growth characteristic of carcino- 
mata. In this border region a certain degree of individual bias must 
be permitted in assigning a name to the new growth. In some cases 
a sharp distinction cannot be made, or the tumor may share in the 
characteristics of both, and then we very properly make use of the 
term adeno -carcinoma or carcino-adenoma. 
23 



330 



TUMORS. 



I. ADENOMA. 

The structure of the cellular elements of these tumors, and theii 
arrangement into acini and ducts, vary even more than do those o\ 
the normal glands whose types they follow. The acini usually pos 
sess a more or less well-defined lumen and membrana propria (set 
Fig. 146). The adenomata sometimes merge into the surrounding 
tissue, or are continuous with the gland tissue in which they ori 
ginate ; sometimes they are distinct in outline and encapsulated 
The interstitial tissue is sometimes abundant, sometimes sparse, anc 
may contain few or many cells. The irregularities of their growtl 




Fio. 146.— Adenoma of Mamma. 



often lead to the stoppage of the lumina of their ducts and the forma 
tion of cysts. They may undergo mucous metamorphosis and maj 
become sarcomatous. 

Adenomata occur in the mamma, ovary, liver, kidney, thyroid 
salivary, and lachrymal glands, and in the caruncle ; in the mucoui 
membrane of the nose, pharynx, stomach, intestine, and uterus ; anc 
occasionally in the sebaceous and sweat glands of the skin. The so 
called multilocular cystomata of the ovary are among the most im 
portant of the adenomata. There are numerous papillary and poly 
poid growths, in gland ducts and on mucous membranes, in whicl 
there is an actual new formation of gland epithelium; but this is usu- 
ally secondary to a primary growth, beneath the epithelial layer, oi 



TUMORS. 331 

some other tissue, such as fibrous or mucous tissue, and the new 
growth of gland epithelium simply keeps pace with the growth of the 
latter, to which it serves as an investment. Such growths are some- 
times classed among the adenomata, but do not, strictly speaking, 
belong there. 

The adenomata are in general benign tumors, being slow of 
growth and localized, but there are very important exceptions. 
Some of the adenomata of the stomach and intestines belong to the 
most malignant of tumors in rapidity of local extension, in the for- 
mation of metastases, and the development of cachexia. Certain of 
the adenomata of the mamma and thyroid are also very malignant. 
It should be remarked, however, that, as a rule, the malignant adeno- 
mata are those which, in structure, lie close upon the border line 







^n^ 



Fig. 147.— Adenoma of Stomach. 
A form which is on the border line of carcinoma. 

between tumors of this class and carcinomata (see Fig. 147), and by 
such observers as incline to lay more stress upon clinical than mor- 
phological distinctions they are usually classed among the latter. 

Adenomata are not infrequently of such bizarre types that their 
nature is not evident without very thorough study. Some of the 
atypical forms lie very close to the border zone of the carcinomata. 

n. CARCINOMA. 

The tumors of this highly important class are composed, as above 
stated, of a connective-tissue stroma, forming more or less well- 
defined communicating spaces or alveoli, in which lie variously 
shaped epithelial cells arranged in an atypical manner. The stroma, 



332 TUMORS. 

containing few or many cells, may be, especially in the advancing 
portions of the tumor, composed largely of the old connective tissue 
of the part. It may, however, be entirely new formed. The cells 
which lie in the spaces or alveoli bear sometimes a very close, some- 
times but a very general resemblance to epithelium. 

It was formerly believed that new epithelium might be formed, 
both from old epithelial cells and from the connective-tissue cells, 
and possibly from white blood cells, and among many observers this 
belief still exists and has never been disproved. Still, within the last 
twenty years the opinion that new epithelial cells in tumors arise 
exclusively from old epithelium has found general acceptance, and 
for very good reasons. No one has actually seen an epithelial cell 
originate under the microscope, and until this can be done our beliefs 
must rest upon indirect observations. In the first place, all the epi- 
thelial structures in the embryo originate in the archiblastic layers, 
that is, in those layers which are largely characterized by the pre- 
sence of epithelium (see page 294). In regeneration after an injury 
in the adult, a study of the successive phases of the process shows 
that new epithelium is always formed in continuity with the old, and 
apparently by a proliferation of old epithelial cells. Epithelial tu- 
mors are almost exclusively found in parts normally containing epi- 
thelium, and frequently the new growth can be distinctly seen to be 
continuous with the old cells. 

Finally, the observations on mitosis have greatly strengthened the 
view that new epithelial cells in tumors are always derived from 
the old. • 

The occurrence of primary epithelial tumors in parts of the body 
in which epithelium does not normally occur, as in bone and the 
lymph nodes, has been recorded; but these may have been metasta- 
tic tumors, in which the primary tumor was small and overlooked, 
or they may have been displaced embryonic germs, which, according 
to Cohnheim's hypothesis (see page 290), would explain their hetero- 
logous occurrence. These possibilities of error should be taken into 
the account in the apparently exceptional cases, and it is to be re- 
marked that these are becoming less and less as our knowledge in- 
creases and our technical facilities for research improve. 

A considerable number of the tumors formerly described as 
heterologous primary carcinomata are now known to be formed by 
proliferation of endothelium, and hence to belong to anot ier class — 
endothelioma — although sometimes considerably resembling the car- 
cinomata in structure. 

The occurrence of primary carcinoma of the peritoneum, pleura, 
and pericardium, which is not infrequent, was for a long time inex- 
plicable, and seemed wholly inconsistent with the belief that all car- 



TUMORS. 



333 



cinomata originate in epithelial cells. Because it was, and to a large 
extent still is, believed that the flat cells lining these great body cav- 
ities are true endothelium, and closely related in origin, as they are 
in structure, to the genuine endothelium of the blood and lymph ves- 
sels, etc. 

But recent embryological researches have shown that this belief 
is not well founded. It was formerly thought that the great serous 
cavities were large lymph vessels formed by the splitting apart of 
the connective-tissue layers of the mesoblast. But we now know 
that the great primitive body cavity, which after a time becomes di- 
vided into the pleural, pericardial, and peritoneal sacs, is originally 




Fig. 148.— Cancer Cells infiltrating the Tissue in the Vicinity of a Tumor. 
From carcinoma mammae. 

an outgrowth from the alimentary canal. The epithelium of the ali^ 
mentary canal, however, is of archiblastic origin, while the connec- 
tive tissue, blood and lymph vessels are developed later from the 
parablast. Genetically, therefore, the so-called endothelial cells lin- 
ing the pleural, pericardial, and peritoneal cavities are of archiblastic 
origin and belong among the epithelium. Thus a fuller knowledge 
of the histogenesis of the cells lining the great body cavities has 
shown us that the occurrence of primary carcinoma in these cavities 
is not only not in contradiction with the principle of the epithelial 
origin of carcinoma, but strongly confirmatory of it. 



334 TUMORS. 

A great practical difficulty in the description, and, to beginners, 
in the recognition, of the carcinomata and their varieties, lies in the 
great diversity in shape which their cells present. It should be 
always borne in mind that the shape of cells depends in part upon 
their inherited tendencies in growth, which we cannot see under 
the microscope; but to a greater degree upon the varying conditions 
of nutriment and pressure to which they are exposed during life. 
In the normal body these conditions conform to a certain standard, 
so that cells of a given kind at a given stage of development are 
approximately similar. 

In tumors, however, the lawlessness and lack of fixed conditions 
in growth are such that we may have many young and atypical so- 
called indifferent forms of cells ; while even the adult forms may 
depart widely from normal shapes. Thus, in cylindrical-celled carci- 
nomata there are many fully developed cells which are never cy- 
lindrical ; there are many others not fully developed which are quite 
indifferent in form, looking just like many other young cells — cells 
which are not, but which are destined to become, epithelium. 
Finally, we have the cells produced by ordinary inflammatory pro- 
cesses about and within the tumor, which acts like an irritating 
foreign body. Thus it is that there is no morphologically charac- 
teristic " cancer cell," as was formerly supposed. Some of them are 
typical and some not, and the more typical ones may look just like 
normal epithelial cells, and the atypical ones just like simple inflam- 
matory cells, or young connective-tissue cells, or white blood cells. 
It is always in the topography, together with the general characters 
of the cells and the situation of the growth, that we must seek for the 
evidences of the nature of a given tumor. 

The carcinomata are very prone to local extension, the advancing 
tumor cells in. the periphery making their way through the lymph 
spaces and forming new foci (Fig. 148) . Metastasis is of frequent 
occurrence in some forms, and takes place chiefly, though not ex- 
clusively, through the lymph vessels, frequently involving adjacent 
or remote lymph nodes. The growth of the tumor cells in the lymph 
vessels, either in the immediate vicinity of the original tumor or fol- 
lowing metastasis in a distant part of the body, may cause these to 
become distended, and, on free surfaces like the pleura and peri- 
toneum, to form a whitish, elevated network. Transverse sections of 
such distended lymph vessels are shown in Fig. 149. The secondary 
tumors are in the main similar in general structure to the primary 
foci, but may differ from them in vascularity and the abundance of 
the stroma, or in the shape of the cells. The carcinomata are, as a 
rule, malignant tumors, but the different forms vary much in this 
respect. They are liable to fatty, colloid, mucous, and amyloid de- 



TUMORS. 335 

generation, and are especially prone to ulceration, to hemorrhage, 




Fio. 149.— Metastatic Carcinoma in Lymph Vessels op the Pleura. 
(The primary tumor was in the liver.) 

and simple inflammation (Fig. 150). They may become partially cal- 
cified, and are not infrequently combined with other forms of tissue 
in the mixed tumors. 



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Fig. 150.— Inflammation in Carcinoma. 
Showing pus cells in the stroma and in the epithelium. 

They are more frequent in middle and old age than in the young, 
but they may occur at any age. 



33G TUMORS. 

Forms of Carcinoma. — In oertain cases of carcinoma which 
occur in the skin and in some mucous membranes, the cells present 
the structure and general characters of the epithelium of the part in 
which they occur ; and since here the tendency of the cells as they 
approach the surface is to become flattened or squamous, these tumors 
are called Squamous or Flat-celled Carcinomata, or simply Epithe- 
liomata. 

In another class of tumors, such as frequently occur in the gastro- 
intestinal canal and uterus, the cells are more or less cylindrical in 
shape, forming a palisade-like lining to the irregular alveoli ; such 
tumors are called Cylindrical-celled Carcinomata, although here 
again many of the cells are not cylindrical at all, but may have a 
great variety of forms. 

There is a third and very common form of tumor, in which the 
epithelial cells have no constant characteristic shape, but vary as 
much as do the cell forms in the various glands of the body. Such 
tumors are conveniently classed together as Gland-celled Carcinoma, 
or Carcinoma simplex. 

In addition to these forms there are several others which depend 
for their characteristics upon various metamorphoses or degenera- 
tions, or upon the preponderance of one or other of the anatomical 
constituents of the growth. It will be most convenient to give a brief 
description of these various kinds, one after another, with the under- 
standing that they are not absolute specific forms, but are simply 
varieties which it is convenient to recognize for clinical as well as 
anatomical purposes. 

Flat-celled Carcinoma, or Epithelioma. — These tumors occur in 
the skin and in the mucous membranes which are covered with 
squamous epithelium. The cells present all of the various forms 
which normally exist in these parts — the cuboidal and polyhedral cells 
of the rete Malpighii, as well as the more superficial flattened forms 
(Fig. 151). Frequently the spined cells, or so-called "prickle cells/' 
are largely reproduced. Having to a certain extent the same life 
history as the cells in which they originate, many of the tumor cells 
become dry, thin, and horny, like the epidermis cells, as they grow 
older ; and since their growth and changes often occur within the old 
lymph spaces of the affected tissue or in the new-formed alveoli, the 
cells are sometimes packed together in spheroidal, concentric masses 
called "epithelial pearls" (Figs. 151 and 154), which may sometimes 
be seen with the naked eye upon or near the surface of the growth. 
The new cell masses may be large or small, may be separated by 
much or little stroma; often form reticular masses, and may infiltrate 
the tissues deeply or remain near the surface ; or may project above 
the surface, forming wart-like or papillary growths. These tumors 



TUMORS. 



33? 



frequently ulcerate on the surface, and the skin about them is apt to 
become thickened (Fig. 153). 




Fig. 151.— Epithelioma of the Neck. 
Shows epithelial pearls, spined cells, and reticular masses of variously shaped epithelial cells. 

(Am 




Fig. 15?.— Metastatic Carcinoma (Epithelioma) in a Lymph Node. 
The primary tumor was in the vagina ; showing at the right a small " epithelial pearL 1 
o ) 



338 



TUMORS. 



They are most apt to occur in the skin, especially in those parts in 
which it becomes continuous with mucous membranes — lips, exter- 




Fig. 153.— Epithelioma of Back of Hand. 
The flat tumor occupied nearly the entire back of the hand, and was ulcerating at the centre. 
The figure shows the edge of the tumor and a portion of the ulcer. The papillae of the skin over 
the edge of the growth are hyper fcrophied, and the tissue about infiltrated with small spheroidal 
cells. Fig. 154 shows a section from a metastatic tumor of the axillary lymph node in this case. 

nal nasal openings, eyelids, labia, and glans penis— and are frequent 
in the mouth, oesophagus, vagina, and about the cervix uteri. 

There are also carcinomata of the skin, composed of cuboidal cells 




Fig. 154.— Epithelioma of Axillary Lymph Node. 
This metastatic tumor was secondary to a large epithelioma of the back of the hand, Fig. 
153. The small cells with darker nuclei are the cells of the lymph node. It shows the epithelial 
pearls. 



TUMORS. 



339 




Fig. 155.— Section of a Portion of a Small Epithelioma of the Side of the Nose. Low 

power. 



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Fig- 156.— Epithelioma of Nose. 
A portion of the tumor shown in Fig. 155 more highly magnified. 






m 






340 



TUMORS. 



arranged in tubules or masses, which do not follow the type of the 
epithelium of the skin, but rather that of the sweat glands or seba- 
ceous glands. These tumors are found most frequently on the nose 
and eyelids (Figs. 155 and 156). 

Sometimes certain of the cells in an epithelioma appear to coal- 
esce, forming a large multinuclear mass. This variety of epitheli- 
oma is sometimes called giant-celled epithelioma. 

Flexner 1 has described a rare tumor arising from the epithelia] 
layers of the retina, which he calls a neuro- epithelioma. 

Epitheliomata are apt to recur if not thoroughly removed, and 
may form metastases, but in general they are the least malignant of 
the carcinomata. The prognosis is in most cases good if there is 
early and complete removal. 

Cylindrical-celled Carcinoma. — These tumors, closely allied tc 



*f#> 









^->- ';■<'** W/M 



Fig. 157.— Carcinoma Mamjle (Scirrlius variety). 

some forms of adenoma (see Fig. 147), occur in the stomach, intes- 
tines, and uterus. The cells may be only in part cylindrical, the re- 
mainder having various shapes, and all being loosely or closely packed 
in larger or smaller alveoli. Th.3y may have much or little stroma. 
They merge imperceptibly into the next class : 

Gland-celled Carcinoma, or Carcinoma simplex. — These, which 
are by far the most frequent of the carcinomata of internal parts, are 
characterized by the alveolar structure and by the absence of anj 
special characteristic shape in the cells, which may be spheroidal, 



1 Flexner, " A Peculiar Glioma (neuro -epithelioma) of the Retina," Johns Hopkim 
Hospital Bulletin, August, 1891. 



TUMORS. 



341 



polyhedral, fusiform, or cuboidal. They may or may not resemble the 
epithelium of the gland in which they originate. They are usually 
nodular tumors, and may be hard or soft. If the stroma is abundant 
and dense, and preponderates over the cellular elements, the tumor is 
usually hard and is called scirrhus or ftbro-carcinoma (Fig. 157). 
If, on the other hand, the cellular elements largely preponderate, the 
tumor is usually soft, and, if it do not contain too many blood ves- 
sels, may have a general resemblance to brain tissue, and is then 
called encephaloid or medullary cancer ; or, better, Carcinoma 
molle (Fig. 158). These are among the most malignant of the car- 
cinomata. 




Fig. 158.— Medullary Carcinoma of the Stomach (Carcinoma molle). 



The intercellular tissue in these carcinomata may become so abun- 
dant as to nearly obliterate the cellular elements, but it is doubtful 
if they ever undergo spontaneous cure in this way. These tumors 
may be hard in one portion and soft in another. They may contain 
very many blood vessels, C. telangiectoides. They occur as primary 
tumors in the mamma, liver, thyroid, salivary, and prostate glands, 
in the pancreas, kidney, testicle, and ovary. 

Colloid Carcinoma. — The cells of certain carcinomata, especially 
of the gastro-intestinal canal, may suffer a more or less complete infil- 
tration with a translucent material somewhat resembling gelatin and 
called colloid, whose nature is not well understood. Sometimes this 



342 



TUMORS. 



infiltration is only partial, when the protoplasm of the cells may be 
more or less encroached upon by the translucent droplets of the col- 
loid material ; but in other cases, over large areas the cells are par- 




Fig. 159.— Colloid Carcinoma op Rectum. 



tially or entirely destroyed, and replaced by the new material, so that 
the alveoli of the tumor are distended by it, and their walls appear 



^^t4vw^(' PIP) 
lib,, i.fftjvjk^^ 









WiBmm 




Fig. 160.— Carcinoma myxomatodes Mamkle. 



very distinct in the midst of the colloid substance (Fig. 159). In such 
cases the alveolar structure of the tumor is sometimes very evident 
to the naked eye, and these tumors are therefore often called alveolar 



TUMORS. 343 

carcinoma. Sometimes only a part of the tumor is affected in this 
way. 

Carcinoma my xomat odes. — The cellular elements of carcinomata 
may suffer mucous softening, and thus larger and smaller cysts 
containing a mucous fluid are sometimes formed. To this form 
of metamorphosed tumor the above name is sometimes applied, but 
it more properly belongs to carcinomata in which the stroma is com- 
posed of mucous tissue (Fig. 160). Such tumors are most frequently 
found in the gastro-intestinal canal and mamma. 

Melano- Carcinoma.— Tumors of this class are rare, and are cha- 
racterized by the presence of a variable quantity of black or brown 
pigment particles either in the stroma or in the cells. They are 
usually soft and malignant, and most frequently occur in the skin. 1 

1 Bibliography. — The most extensive and important work on tumors, containing 
a vast store of information, is that of Rudolph Virchow, " Die krankhafte Ge- 
schwiilste." It is not completed and is somewhat old, but is still invaluable as a work 
of reference. The section on tumors in Von Pitha and Billroth's work on surgery 
(" Handbuch der allgemeinen u. speciellen Chirurgie "), which comprises the first sec- 
tion of the second volume, by Dr. Lucke, is very complete. A valuable bibliography 
and digest of recent observations on tumors will be found in the last edition of Birch- 
HirschfeWs work on pathological anatomy (" Lehrbuch der pathologischen Ana- 
tomie "), vol. i. ; also in Ziegler's " Lehrbuch der path. Anat.," Band i., 7th ed., 1892. 
An important resume on the Malignant Tumors in Childhood, by Stern, maybe found 
in the Deutsche med. Wochenschrift, June 2d, 1892, p. 494. " An Introduction to 
General Pathology, " by Sutton, contains many suggestive facts about tumors drawn 
from comparative pathology. 



PART III. 

PATHOLOGICAL ANATOMY AND HIS- 
TOLOGY OF THE ORGANS. 



THE JSTEKVOUS SYSTEM. 



THE MEMBRANES OF THE BEAIN. 

THE DURA MATER. 

The dura mater is a dense connective-tissue membrane which 
serves the double purpose of a periosteum for the inner surface of 
the cranial bones, and of an investing membrane for the brain. It 
is itself but poorly supplied with blood vessels, but it contains the 
large venous sinuses which carry the blood from the brain. Lesions 
of the dura mater, therefore, are apt to be associated with lesions of 
the cranial bones, of the pia mater, or of the venous sinuses. 

In young children the dura mater adheres closely to the inner 
surface of the cranial bones, in adults it is more readily detached, 
and in old persons it is again more adherent. Chronic inflammation 
of the external layers of the dura mater also renders it more adherent 
to the bones. 

HEMORRHAGES. 

We find extravasations of blood between the dura mater and 
the cranial bones, in the substance of the membrane, and between the 
dura mater and the pia mater. 

The haemorrhages in the substance of the dura mater are usually 
small and of little consequence. 

The haemorrhages between the dura mater and the pia mater oc- 
cur with chronic pachymeningitis, or are derived from the vessels of 
the pia mater. 

The haemorrhages between the dura mater and the cranial bones 
are produced by blows and injuries of the head. They are often of 
considerable size, separate the membrane from the bones, and may 
compress the brain. They are often associated with laceration of 
the brain, and haemorrhages between the dura mater and pia mater. 

The pressure on the head of the infant in labor may produce, in 
addition to the extravasations of blood between the bones and the 
pericranium, additional extravasation between the bones and the 
dura mater. 



348 THE NERVOUS SYSTEM. 

THROMBOSIS. 

Thrombosis of the venous sinuses is not uncommon. Any i 
flammation of the dura mater is liable to produce it ; injuries and i 
flammations of the brain and pia mater, of the cranial bones, of t 
middle ear, and of the scalp may also produce thrombosis. T 
changes in the blood produced by the exhausting and infectious di 
eases may induce thrombosis of the venous sinuses, as they do 
the veins in other parts of the body. There are also rare cases 
which such a thrombosis is developed without discoverable cause 
persons previously healthy, and produces marked symptoms ai 
death. 

Some of these thrombi are firm, of white or red color, and a 
parently produce no secondary lesions. 

Others are of firm consistence, but they produce softening wi 
small haemorrhages of portions of the brain. In these cases tl 
thrombus extends from the venous sinus into one of its veins, ai 
the portion of brain belonging to this vein is softened and haemc 
rhagic. Such a softening of the brain is often attended with i 
flammation of the pia mater. 

In other cases the thrombi are soft and purif orm ; fragments 
them become detached and lodge as infectious emboli in the arteri 
in different parts of the body. 

INFLAMMATION. 

Inflammation of the dura mater is called pachymeningitis, ar 
this may involve the external layers of the membrane, pachymeni 
gitis externa, or the internal layers, pachymeningitis interna. 
may furthermore be either acute or chronic. The tissues of the su 
stance of the dura mater participate to a greater or less degree 
these changes, but the chief lesions are upon the surfaces. 

Acute pachymeningitis externa is usually secondary to injuri 
or diseases of the cranial bones ; thus fractures of the skull, eith 
depressed or not, .ostitis, caries, suppurative inflammation of the i: 
ternal and middle ear and mastoid cells, may produce it. The dui 
mater is usually congested, thickened, and softened, and may presei 
small ecchymoses. The inflammation is usually suppurative, ar 
pus may accumulate between the membrane and the bone, or in tl 
substance of the membrane. The areas of inflammation are not usi 
ally extensive. It sometimes induces thrombosis of the venous sii 
uses, and sometimes gangrene of the dura mater occurs. The inflarj 
mation may extend to the inner surface of the dura mater, to the p: 
mater and brain, or it may remain localized and undergo resolutio] 

Acute pachymeningitis interna may be secondary to inflamm; 



THE NERVOUS SYSTEM. 349 

tion of the external surface, or it may occur as a complication in 
pyaemia, puerperal fever, chronic diffuse nephritis, in the exanthe- 
mata and erysipelas, or idiopathically. There is a general or cir- 
cumscribed production of fibrin and pus, so that the internal surface 
of the membrane is lined with a layer of soft, yellow exudation. 

Simple chronic pachymeningitis consists in the formation of new 
connective tissue in the dura mater, by which it becomes thicker 
and in many cases abnormally adherent to the bones of the skull. 
This thickening may be general or circumscribed, and may involve 
the entire thickness of the membrane. Not infrequently, when the 
external layers are especially involved, firm adhesions to the skull 
occur, with ossification of the outer layers, so that shreds of the 
membrane containing little masses of bone (osteophytes) remain 
sticking to the skull when the membrane is stripped off. 

There is an important form of chronic inflammation of the inter- 
nal layer of the dura mater, called pachymeningitis interna hcemor- 
rhagica, characterized by the formation of layers of new delicate 
connective tissue with numerous very thin-walled blood vessels from 
which the blood is prone to escape. The membrane may at first ap- 
pear as a delicate fibrinous pellicle, with small red spots scattered 
through it, or it may look like a simple reddish or brown staining of 
the inner surface of the dura mater. Microscopical examination 
shows this membrane to consist of numerous blood vessels, mostly 
capillaries with very thin walls, which may be distended or pouched, 
and which have grown out from the vessels of the dura mater (Fig. 
161). Between the vessels is a homogeneous or slightly differentiated 
basement substance, containing a variable number of spheroidal, 
fusiform, or branching cells. Red blood cells in variable quantity, 
and blood pigment in various forms, frequently enclosed in the new 
cells, and small calcareous concretions (brain sand) (Fig. 162), also 
lie in the intervascular spaces. In more advanced stages the new 
membrane may become greatly thickened, its outermost layers being 
changed into dense fibrous tissue with obliteration of the vessels ; 
while the more recently formed layers are similar in structure to 
those at first developed. Considerable blood usually escapes from 
the vessels of the new membrane by diapedesis, in all stages of its 
formation, and the vessels are also very liable to rupture, giving rise 
to extensive haemorrhages either into the substance of the membrane 
or between it and the pia mater. Sometimes masses of new tissue 
and blood, from half an inch to an inch or more in thickness, are in 
this way formed, greatly compressing the brain. These new mem- 
branes are most frequently formed over the convexity of the brain, 
but may extend over nearly the entire surface of the dura mater. 
Sometimes, when old, the entire membrane, densely pigmented and 



350 



THE NERVOUS SYSTEM. 



firm, lies loosely beneath the dura mater without compressing tl 
brain or giving any clinical indication of its presence. The meE 
brane may induce chronic changes in the pia mater, with or withoi 
accompanying changes in the cortical portion of the brain. 




'7: 
Fig. 161 —Chronic Pachymeningitis interna hemorrhagica. 



Rarely, serum accumulates between the layers of the new men 
brane, and in this way cysts of large size may be formed. In rai 
cases diffuse suppuration of the entire new membrane occurs. 




Fig. 162.— Brain Sand from Pachymeningitis interna. 



The slighter degrees of this form of inflammation may occasio: 
no symptoms during life. They are not infrequently found in pei 
sons suffering from various chronic brain lesions and from chroni 
alcoholism, but they may occur unassociated with complicating lesions 



THE NERVOUS SYSTEM. 351 

The more advanced forms of the lesion are frequently found in idiots, 
epileptics, etc. 

Tuberculous pachymeningitis may occur secondarily to that form 
of inflammation in the pia mater or the bones, or as a part of general 
miliary tuberculosis. The tubercles may be situated on either sur- 
face of the membrane or in its substance, and may be single or aggre- 
gated, forming large masses. 

Syphilitic pachymeningitis manifests itself by the formation of 
so-called gummy tumors upon either the external or internal surface 
of the dura mater. These tumors may be single or multiple, and 
vary greatly in size, They may be accompanied by simple inflam- 
matory changes in the dura mater in their vicinity. They may 
undergo suppuration with the formation of abscess ; the inflammation 
may extend to the pia mater, inducing simple or syphilitic meningi- 
tis and adhesions between the dura mater and pia mater. The gum- 
mata may, on the other hand, when occurring on the outer surface 
of the membrane, cause absorption and perforation of the bones of 
the skull. 

TUMORS. 

The most common tumors of the dura mater are sarcomata, and 
of these the spindle-celled forms are of more, the round- and polyhe- 
dral-celled of less frequent occurrence. They may grow from either 
surface of the membrane. Some of the round- and polyhedral-celled 
forms are soft and very vascular, and are apt to involve the neigh- 
boring pia mater and brain tissue, or the bones of the skull, which 
they may perforate. They sometimes project through the opening 
in the skull in fungous, bleeding masses. 

Psammomata are small globular tumors, often multiple and 
pediculated, growing from the inner surface of the dura mater. 
They are usually composed of tissue sarcomatous in character, and 
contain variously shaped calcareous concretions similar in appearance 
to the so-called brain sand. 1 

Endotheliomata. 2 — These tumors may grow inward or outward, 
causing pressure on the brain or absorption and perforation of the 
bones ; they often attain considerable size. Some of these tumors 
somewhat resemble certain forms of epitheliomata (see Fig. 116), and 
have often been described as primary carcinomata. 

Fibromata and Lipomata occur rarely in the dura mater and 
are of small size. 

1 For a study of psammoma consult Ernst, " Ueber Psammoraa, " in Ziegler's Bei- 
trage zur path. Anatomie, Bd. xi., page 234, 1892. 

a For a consideration of tumors of the dura mater allied to the endotheliomata con- 
sult Dogonet, Arch, de Med. Exp., May 1st, 1892. 



352 THE NERVOUS SYSTEM. 

Small Chondromata are sometimes found connected with the 
dura mater at the base of the brain. 

Osteomata. — In addition to the formation of osteophytes in 
chronic external pachymeningitis, plates and, more rarely, globular 
masses of bone may be formed in the dura mater, unconnected with 
the bones of the skull. They are most frequently found in the falx 
cerebri, but may occur elsewhere. The new bone may be dense or 
loose in texture, and usually produces no symptoms. 

THE PIA MATER. 

The external surface of the brain is invested by a connective-tis- 
sue membrane which covers the convolutions, dips down into the 
sulci, and extends into the ventricles. This membrane is abundantly 
supplied with blood vessels, and from it numerous vessels extend into 
the brain, so that any disturbance in the circulation of the blood in 
the pia mater involves a disturbance in the circulation of the blood 
in the brain also. 

The connective tissue which makes up the pia mater is arranged 
in a series of membranes and fibres reinforced by elastic tissue, so ar- 
ranged as to form a spongy membrane containing numerous cavities 
more or less filled with fluid. These cavities are continuous with the 
perivascular spaces which surround the vessels that pass from the pia 
mater into the brain. 

The outer layers of the pia mater are the most compact, and are 
covered on their outer surface by a continuous layer of endothelial 
cells. This external layer of the pia mater is often described as a 
separate membrane called the " arachnoid," but it is really only part 
of the pia. 

The deeper layers of the pia contain the blood vessels. The mem- 
branes and fibres which compose the pia mater are partly coated with 
cells which have irregular and delicate cell bodies and large, dis- 
tinct nuclei. 

In all inflammations of the pia mater the inflammatory products 
regularly collect in the spaces within it. 

Along the borders of the longitudinal fissure, and, more rarely, 
on the under surface of the brain, are a number of small, white, firm, 
irregular bodies — the Pacchionian bodies. They vary in their size, 
their number, and in the extent of the surface of the hemispheres 
which they cover. They may perforate the dura mater, or, more 
rarely, the wall of the longitudinal sinus, and may produce erosions 
of the skull bones. They are composed of fibrous tissue and may un- 
dergo fatty or calcareous degeneration. As they are so commonly 
found and are not known to be of any pathological significance, they 



THE NERVOUS SYSTEM. 353 

may almost be regarded as normal structures ; at any rate, we do 
not know what causes them or their variations in size and number. 

The pia mater is frequently thickened, opaque, and white, either 
in diffuse patches or, more commonly, along the course of the ves- 
sels. In other cases single or multiple small white spots, of the size 
of a pin's head or smaller, may be seen in the membrane, not appre- 
ciably elevated above the surface, but due to localized thickening. 
These slight opacities of the pia mater are commonly believed to be 
dependent upon repeated congestions of the membrane or upon 
chronic meningitis, but there is no evidence that this is always the 
case. They are most frequently found in old persons, but may exist 
at any age, and do not necessarily indicate the pre-existence of dis- 
ease, although similar appearances are common in the chronic insane 
and in drunkards. 

The amount of blood contained in the vessels of the pia mater af- 
ter death varies greatly, and is by no means a reliable indication of 
the amount present during life. In general anaemia the vessels of 
the pia mater may contain little blood, but, on the other hand, they 
sometimes seem to contain a relatively larger amount than other 
parts of the body. In oedema of the brain and pia mater the vessels 
of the latter may contain but a small amount of blood. 

CEDEMA. 

The quantity of serum beneath the pia mater and infiltrating 
its tissue is very variable in amount. It may accumulate as a 
result of atrophy of the brain substance or of venous hypersemia, 
and sometimes is, and sometimes is not, accompanied by oedema of 
the brain substance. It may be diffuse or localized. It is not infre- 
quent to find in hospital patients suffering from chronic nephritis, 
cardiac or pulmonary disease, or chronic alcoholism, a very consid- 
erable amount of serum in this situation, and yet the patient has 
been free from cerebral symptoms. In other cases, again, a serous 
effusion may accompany grave cerebral symptoms. It is necessary 
to be very careful in judging of the importance of this accumulation 
of fluid, especially in determining the cause of death in the absence 
of Other marked lesions (see page 373). 

It should always be borne in mind that an accumulation of fluid 
beneath and in the meshes of the pia mater may occur as a result of 
post-mortem changes. 

HYPEREMIA AND HEMORRHAGE. 

The pia mater may be hypercemic in early stages of meningitis, 
after death from delirium tremens or following epileptic convul- 



I 

354 THE NERVOUS SYSTEM. 



sions, from various infectious diseases, certain poisons, the presence 
of tumors or exuaations pressing on the veins, as well as from gen- 
eral and local diseases of the circulatory apparatus. But whether 
they are overfilled or comparatively empty after death seems to de- 
pend upon the position in which the body has lain, upon the time 
which has elapsed between death and the examination, upon the 
rapidity with which the blood coagulates, and upon conditions en- 
tirely unknown to us. 

Hcemorrhage. — This may occur either into the space between the 
dura mater and the pia mater — inter meningeal hcemorrhage — or in 
the meshes of the pia or between the latter and the brain. It may 
be due to injury, to rupture of aneurisms or otherwise diseased blood 
vessels, to thromboses of the venous sinuses, or to causes which we are 
unable to ascertain. Haemorrhages, without known cause, not infre- 
quently occur in the substance of the pia mater in young children, 
but in adults they are apt to be the result of injury. Multiple ecchy- 
moses, however, in the substance of the pia mater sometimes occur 
in infectious diseases and also in acute inflammation of the pia mater. 
Haemorrhages in the brain substance may lead to the accumulation of 
blood beneath or in the meshes of the pia mater. Intermeningeal 
haemorrhage in infants as a result of injury during birth is not un- 
common. Small, and sometimes considerable, extravasations of blood 
may occur from diapedesis, and sometimes, as a result of chronic 
congestion, degenerated blood pigment collects along the walls of 
the vessels. The extra vasated blood in meningeal haemorrhage, if 
small in quantity, may be largely absorbed, leaving a greater or 
smaller accumulation of pigment at the seat of the haemorrhage, and 
such pigmentations may last for a long time. 

INFLAMMATION. 

Inflammation of the pia mater is called lepto-meningitis, or sim- 
ply meningitis. We distinguish acute, chronic, tubercular, and syph- 
ilitic meningitis. 

Acute Meningitis occurs most frequently as the characteristic 
lesion of epidemic cerebro-spinal meningitis ; it is a not very infre- 
quent complication of pneumonia, Bright's disease, typhus and ty- 
phoid fever, and the exanthemata ; it is secondary to injuries and 
inflammation of the cranial bones, of the dura mater, and of the 
middle ear, and it is sometimes an idiopathic lesion (see page 200). 

In acute meningitis the inflammation is apt to extend downward 
and involve the pia mater of the cord. It may also involve the epen- 
dyma of the ventricles, and cause the distention of these cavities with 
serum. This latter condition belongs especially to young children. 



THE NERVOUS SYSTEM. 



355 



There are two anatomical varieties of acute meningitis, which 
give, however, the same clinical symptoms. 

(1) Acute Cellular Meningitis. — The pia mater is congested, 
its surface is dry and lustreless, and it is somewhat opaque. 
These changes in the gross appearance of the membrane are not 
marked and are easily overlooked, but the minute changes are more 
decided. There is an abundant production of cells somewhat re- 
sembling the cells which coat the surfaces of the membranes and 
fibres which make up the pia mater (Fig. 163). This cell growth is 




Fig. 163.— Acute Cellular Meningitis, X 850 and reduced. (Surface view. ) 



general, involving the pia mater over most of the surface of the brain. 
The inflammation, then, is one which results in the production, not of 
fibrin, serum, or pus, but of new connective-tissue cells. This form 
of meningitis is of frequent occurrence and is attended with the ordi- 
nary clinical symptoms of acute meningitis. 

(2) Acute exudative meningitis is characterized by the accu- 
mulation, chiefly in the meshes of the pia mater and along the walls 
of the blood vessels, of variable quantities of serum, fibrin, and pus. 
Sometimes one, sometimes another of these exudations preponde- 
rates, giving rise to serous, fibrinous, or purulent forms of the in- 
flammation. The absolute quantities, too, of the exudations vary 



356 



THE NERVOUS SYSTEM. 



greatly. In some cases death may be caused with so slight a for- 
mation of exudation that to the naked eye the pia mater may look 
quite normal or perhaps only moderately hypersemic or cedematous ; 
the microscope, however, in these cases will reveal pus cells in small 
numbers (Fig. 164) and sometimes flakes of fibrin in the meshes and 



m 




Fig. 164.— Acute Meningitis. 
Proliferation of connective tissue cells and extravasation of leucocytes in the adventitia of a 
small blood vessel of the pia mater. 

along the walls of the vessels. In other cases turbid serum in the 
meshes of the membrane is all that can be seen, and the microscope 
shows the turbidity to be due to pus cells or a small amount of fibrin. 
Again, either with or without marked oedema of the pia mater, yel- 
lowish stripes are seen along the sides of the veins, sometimes ap- 
pearing like faint turbid streaks, and at others dense, opaque, thick, 
and wide, and almost concealing the vessels. These are due to the 
accumulation of pus cells and fibrin in large quantities along the ves- 




^Usses^- 



Fig. 165.— Acute Exudative Meningitis. 
a, convolutions of cerebrum ; 6, pia mater thickly infiltrated with pus ; c, blood vessels entering 
brain from pia and surrounded by a zone of pus cells ; d, congested blood vessels of pia mater ; e, 
smaller blood vessels of pia, around which pus cells are collected in dense masses. 



sel, and they are best seen and most abundant around the larger veins 
which run along over the sulci. In still other cases the infiltration 



THE NERVOUS SYSTEM. 



357 



with pus and fibrin is so dense and thick and general that the brain 
tissue, convolutions, and most of the vessels of the pia mater them- 
selves are concealed by it. This is usually of a greenish-yellow 
color, and is sometimes so thick as to form a sort of cast of the brain 
surface at the seat of the lesion (Fig. 165). Sometimes extravasated 
red blood cells are mingled with the other exudations, as the result of 
diapedesis. Microscopical examination shows numerous white blood 
cells sticking in the walls of the veins and capillaries, or the vessels 
may be blocked with them. It is evident that a large part of the 
pus cells accumulate as the result of emigration. The connective- 
tissue cells of the pia mater may be detached from their places or 




Fig. 166.— Fatty Degeneration of Cells along the Blood Vessels of the Pia Mater 
after Exudative 3Ientngitis. 

From the pia mater of a child five years old. 

degenerated. In some cases there are considerable accumulations of 
pus between the pia mater and the brain substance and along the 
vessels which enter the latter. More rarely pus is found upon the 
free surface of the membrane. The brain substance may be com- 
pressed by the accumulated exudation, so that the convolutions are 
flattened. The cortical portion of the brain may be simply infiltrated 
with serum — cedematous — or it may undergo degenerative changes, 
or it may be the seat of punctate haemorrhages. Not infrequently 
the inflammation extends to the ventricles, which may contain puru- 
lent serum, and to the pia mater of the cord. This form of inflam- 
mation is most frequent on the convexity of the brain, but may ex- 



!58 



THE NERVOUS SYSTEM. 



tend, or even be confined to the base. It may be localized, but 
frequently extends widely over the surfaces of the hemispheres. 
Bacteria are often present in the exudation. For their relationship 
to the lesions see Cerebro-spinal Meningitis. 

When recovery from acute exudative meningitis occurs there 
may be fatty degeneration of the cells which have accumulated in 
the pia mater, particularly along the vessels (Fig. 166), and this may 
produce white patches in the membrane and threads along the blood 
vessels, which resemble the appearance of an accumulation of exuda- 




Fig. 16? 



-A Miliary Tubercle of the Pia Mater, X 850 and reduced. 
Composed of a simple aggregation of cells. 



(Surface view- 



tion in the acute stage. Fatty degeneration of the blood vessels and 
cells of the pia mater may also occur without acute inflammatory 
changes. 

Sometimes, in children and young adults, inflammatory changes 
in the ventricles persist for days and weeks after the subsidence of 
the inflammation of the pia mater. 

Chronic Meningitis.— Either the pia mater at the base of the 
brain alone may be inflamed (basilar meningitis), or the pia mater 
over the convexity alone, or the entire pia mater, or circumscribed 
patches of the membrane. The pia mater is thickened and opaque, 
the thickening being sometimes very considerable. There is a forma- 
tion of new connective tissue aud a production of pus, fibrin, and 



THE NERVOUS SYSTEM. oO'J 

serum ; the relative quantity of these inflammatory products varies 
in different cases. Firm and sometimes extensive adhesions may be 
formed between the dura mater and the pia mater. Not infrequently 
the cortical portions of the brain participate in the morbid process, 
and we find an infiltration of small spheroidal cells around the blood 
vessels, thickening of the walls of the vessels, and degenerative 
changes and atrophy of the nerve tissue. New connective tissue may 
also form in the brain substance, which may become closely adherent 
to the pia mater. The ventricles of the brain also may contain an 
increased amount of serum and may be dilated, and the ependyma 
may be thickened and roughened. This form of inflammation may 
be the result of injury or disease of the cranial bones, or secondary 
to chronic pachymeningitis or to inflammation of the brain substance. 
It may occur in the vicinity of tumors of the brain or meninges. It 
may be a complication of chronic diffuse nephritis or the result of 
chronic alcoholic poisoning. It may occur in marked form in the 
general paralysis of the insane. 

Tuberculous Meningitis. — This is especially characterized by the 
formation in the pia mater of miliary tubercles, associated with more 
or less well-marked exudative inflammation. It may occur in adults 
and in children, but is more common in the latter. The dura mater 
may be unchanged, or its inner surface may be sprinkled with mili- 
ary tubercles. The pia mater may or may not be congested ; it may 
look dry on the surface or it may be oedematous. Usually the brain 
seems to fill the cerebral cavity to an unusual degree, and the convo- 
lutions are flattened. If the pia mater be oedematous the serum 
may be clear, or turbid with pus and fibrin. The membrane may pre- 
sent any of the general appearances of exudative meningitis. But 
always in addition to these, and sometimes without them, miliary 
tubercles, either widely scattered or in great numbers, may be seen, 
usually more abundant over the sulci than elsewhere. They are 
usually more abundant at the base of the brain than on the con- 
vexity, and are frequently confined to the base. Some of the tuber- 
cles are so small as to be scarcely visible or entirely invisible to the 
naked eye ; others are as large as a pin's head or larger. They are 
usually most abundant along the blood vessels, but may occur else- 
where. They may be formed in the membranous prolongations of 
the pia mater which dip into the sulci, around the vessels which enter 
the brain substance, in the choroid plexus and ependyma of the ven- 
tricles, and may exist in the spinal cord. 

The miliary tubercles do not all have the same structure. Some 
of them are simply small aggregations of round cells within the peri- 
vascular sheaths of the smaller arteries. Others are composed of 
small masses of polyhedral and round cells (Fig. 167) without any 



360 



THE NERVOUS SYSTEM. 



basement substance between them, and without any special relatior 
to the blood vessels. Many others have the ordinary structure oJ 
tubercle tissue, basement substance, polyhedral cells, and giant celk 
(Fig. 168). These tubercles are usually situated around or near 2 
blood vessel, and this blood vessel is apt to be at the same time thc- 




Fig. 168.— Miliary Tubercle of the Pia Mater of a Child, undergoing Cheesy DEGENERi 
tion at its Centre. 

seat of an obliterating endarteritis (Fig. 169). This form of tubercle 
is also prone to cheesy degeneration (Fig. 168). 

In children the ventricles are usually more or less distended by ar 
accumulation of transparent or turbid serum, and the walls of the 
ventricles may be studded with miliary tubercles (see Figs. 170 anc 
171). In adults the ventricles are less frequently involved. The 
brain tissue around the ventricles is often softened. The centra 




Fig. 169.— A Miliary Tubercle of the Pia Mater. 
Situated on the wall of a small artery which is the seat of endarteritis. 

canal of the spinal cord may also be dilated. It is that dilatation o: 
the ventricles which causes the flattening of the convolutions, anc 
the flattening is usually in direct proportion to the amount of accu 
mulated fluid. Miliary tubercles in the choroid of the eye are presen 
in a considerable proportion of cases. 

The cortex of the brain may be hypersemic, and punctate haemor 
rhages may be present in the cortex and in the pia mater. 



THE NERVOUS SYSTEM. 



361 




^^W-#t# 



Fig. 170.— Miliary Tubercles of the Ependyma of the Lateral Ventricle, x 70 and reduced. 







mm 



SiSfiSsS 



% 



m 0sKM , 






m^f 




Fig. 171, — A Miliary Tubercle of the Ependyma of the Lateral Ventricle, magnified, 
X 500 and reduced. 

30 



362 THE NERVOUS SYSTEM. 

In almost all cases of tuberculous meningitis there is tuberculous 
inflammation in other parts of the body. 

In adults, as in children, while the tuberculous inflammation is 
always present, the accompanying simple inflammation may be very 
slight or extensive, and the degree to which it develops does not seem 
to depend upon the abundance of the miliary tubercles. Owing to 
the frequency of the dilatation of the ventricles with serum in chil- 
dren, the disease is often called acute hydrocephalus. 

In both children and adults the tuberculous inflammation may 
produce large masses of tuberculous tissue, which undergo cheesy 
degeneration, in the pia mater and the brain tissue. 

Syphilitic Meningitis. — In this form of inflammation, which is 
usually circumscribed, there is a development of gummy tumors of 
variable size, frequently associated with simple inflammation of the 
membrane, either with the formation of serum, fibrin, and pus, or 
with the development of new connective tissue and the consequent 
thickening of the membrane. The gummata may form in the pia 
mater covering the convexity, or at the base of the brain. They may 
grow outward, involving the dura mater ; or inward, encroaching 
upon or involving the brain tissue. Although usually circumscribed, 
the syphilitic inflammation may occur as a diffuse thickening of the 
membrane. The syphilitic nodules, including the gummata and new- 
formed connective tissue, are often very small, but may be as large as 
a hen's egg. 

TUMORS. 

Hcematoma. — In the cases of chronic pachymeningitis of long 
standing the new connective tissue may form large, flat cysts be- 
tween the dura mater and the pia mater, which may compress the 
surface of the brain. The blood originally contained in these cysts 
may be absorbed and replaced by serum, the attachments to the dura 
mater may disappear, and the whole appearance becomes that of an 
independent cyst between the dura mater and pia mater. 

It is believed by some observers that these cysts are not formed in 
this way, but that they represent a blood clot which has become en- 
veloped in connective tissue. 

Endotheliomata. — These tumors are of not infrequent occurrence, 
and may grow from the pia of the cerebrum or cerebellum or from 
the choroid plexus. 

They may be single or multiple. They may be small or so large 
as to seriously compress the brain. One of us (Delafield) has seen a 
case in which there were several tumors growing in the dura, in the 
pia of both the brain and spinal cord, and from the choroid plexus. 

Some of them are composed of a connective-tissue stroma which 
encloses regular spaces filled with large, flat, nucleated cells. The 



THE NERVOUS SYSTEM. 363 

whole appearance resembles that of an ordinary carcinoma, but the 
cells are apparently of endothelial and not of epithelial origin. 

Some of them are composed of a connective-tissue stroma which 
forms cavities lined with cylindrical epithelium. In such tumors 
the stroma may grow so as to form papillse covered with cylindrical 
epithelium ; or in addition there may be mucous degeneration of the 
stroma. 

In some of them there is a connective-tissue stroma which con- 
tains large numbers of blood vessels. Around these blood vessels are 
arranged regular masses of polyhedral cells (Figs. 172 and 173). 




Fig. 172.— Endothelioma of the Cerebellum Originating in the Pia Mater. 
From a specimen loaned by Dr. Wood. 

In some of them the stroma is scanty. The cells are numerous, 
large, flat, and arranged in little globular masses or nests. 

If in these little nests there is a deposition of the salts of lime, 
forming concretions like the so-called " brain sand/ 7 the tumor is 
called a "psammoma." 

Some of the tumors seem to be formed of very thin, nucleated 
membranes arranged in concentric layers like the layers of an onion. 

Some of the tumors are composed of balls or nests of large, flat 
cells, with which are found crystals of cholesterin — "cholestea- 
toma." 

Sarcoma. — Tumors belonging to the ordinary types of round- and 



364 THE NERVOUS SYSTEM. 

fusiform -celled sarcoma, of myxo-sarcoma, and of myxoma are 
occasionally found in the pia mater. 

Fibromata, lipomata, chondromata, and osteomata are of ran 
occurrence. 

Cysts. — Small cysts are often found in the choroid plexus. Rare 
ly such cysts reach a larger size, even as large as a pigeon's egg. 



c — ^ s ---,,- 




# « 



a 






M ^ , 
^ 



>i~> 



f **- @f - 




o 







42y 



-v .'. * ' ' * - '•"■ ^' : - '* : ■ "^ 

Fig. 173.— Endothelioma of the Pia Mater op the Cerebellum. 
From specimen shown in Fig. 172 more highly magnified. A, Section of pia mater dipping into 
a sulcus; B, tumor cells growing at each side of the pia; C, surface of cerebellar convolutions. 

Cysts of the pia mater containing serum, with walls and septa of 
connective tissue, and compressing the brain, have been described. 

Variously shaped pigment cells not infrequently occur in the pia 
mater, either scattered or sometimes in considerable masses ; they 
seem to have little pathological significance. Not infrequently thin 
plates of new-formed bone are found in the pia mater, associated 
with a thickening of the membrane. 

PARASITES. 

Cysticercus has been observed in the pia mater. 



THE NERVOUS SYSTEM. 305 



THE VENTRICLES OF THE BRAIN. 
THE EPEXDYMA AXD CHOROID PLEXUS. 

As the lymph spaces of the pia mater and the ventricles of the 
brain are in communication, it might be supposed that they would 
share alike in the accumulation of fluids. This, however, is not the 
case. The membranes of the brain may be highly cedematous while 
the ventricles contain about the normal quantity of fluid ; or, on the 
other hand, the ventricles may be widely dilated and the pia mater 
unusually dry. Many of these varying conditions may be under- 
stood by remembering that the skull and spinal canal form a closed 
cavity, and that accumulations of fluid in one part must be at the 
expense of some material occupying other parts, either blood, serum, 
or brain tissue. It is not always easy to see, however, exactly how 
the compensation occurs. 

There may be an unusual amount of fluid in the ventricles of the 
brain as a result of post-mortem change ; in connection with senile 
or other atrophy of the brain, or in the general vascular changes 
which lead to oedema of the brain ; in connection with inflammation 
of the meninges or of the ependyma ; or under conditions which we 
do not understand, as in some cases of congenital and acquired hy- 
drocephalus. Accumulations of fluid in the ventricles are often 
called internal hydrocephalus to distinguish them from accumula- 
tions in the meninges — external hydrocephalus. 

IXFLAMMATIOX. 

Acute Inflammation of the Ependyma (Acute Ependymitis) . — 
In this condition, which may occur by itself, but is usually associ- 
ated with inflammation of other parts of the brain, the ependyma is 
congested, the vessels are more prominent than usual and are often 
tortuous. The ependyma and the adjacent brain tissue may be 
thickened and infiltrated with pus cells, and the surface of the 
ependyma covered with fibrin and pus in variable quantity (Fig. 
174). The cavities of the ventricles may contain purulent serum. 
Small hemorrhages may also be present in the tissue of the ependy- 
ma. This, as well as other forms of inflammation, is more common 
in the lateral ventricles than in the others, but not infrequently in- 
volves the fourth ventricle. The choroid plexus may participate in 
the inflammatory changes of the ependyma. Tuberculous inflamma- 
tion of the ependyma is, as above mentioned, a not infrequent 
accompaniment of tuberculous meningitis. 

Chronic Inflammation of the Ependyma (Chronic Ependy- 



366 THE NERVOUS SYSTEM. 

mitis). — This lesion, which is much more common than simple acute 
inflammation of the ependyma, occurs under a variety of conditions, 
and its nature and causation are in general very obscure. The 
ependyma is thicker, whiter, and more opaque than normal, so that 
the vessels may be nearly or quite invisible. The thickening may 
occur in patches or diffusely, and the surface of the ependyma may 
be smooth, or roughened and granular. On microscopical examina- 
tion the surface of the ependyma may be covered with the usual 
epithelium, but the new connective tissue which forms beneath it 
often raises it up in places, causing the roughness of the surface. 



:-:■■- "■'■■ v->; 




*^% 



mmm0r ,.• • ■;*$ 







Fig. 174.— Acute Ependymitis. 
Showing replacement of the epithelium of the ventricle by inflammatory exudate; collections 
of pus cells near the epithelium and about the adjacent small blood vessels. (From specimen pre- 
pared by Dr. Hodenpyl. ) 

The new tissue is usually rather loose in texture and may contain 
many small spheroidal cells ; but it may be dense in texture and 
contain few cells. The brain tissue beneath the thickened epen= 
dyma may be softened or infiltrated with cells. The sides of the 
ventricles may be grown together in places by the adhesion of the 
thickened and roughened ependyma. The ventricles usually con- 
tain more serum than normal, and sometimes this accumulation is so 
great as to cause an enormous dilatation of them. While these are 
in general the prominent lesions in chronic inflammation of the 
ependyma, the cases vary greatly in the degree to which these 
changes are developed. 



THE NERVOUS SYSTEM. 



367 



The accumulation of fluid and the dilatation of the ventricles 
being the most marked feature in all this class of lesions, they are 
often called chronic hydrocephalus, and indeed in many cases we 
have no evidence that the change in the ependyma is an important 
or even an actual primary factor. 

We may, for convenience of study, consider three classes of cases 
of chronic hydrocephalus : first, congenital hydrocephalus in young 
children ; second, secondary hydrocephalus in children and adults ; 
third, primary hydrocephalus in adults. 




Fig. 175.— Congenital Hydrocephalus in Child. About half natural size . 
a, a, dilated lateral ventricles; b, cornua, unequally dilated ; c. third ventricle; d, middle com- 
missure. 



1. Congenital Hydrocephalus. — The lesion may be in an ad- 
vanced stage at the time of birth, or it may be scarcely evident or but 
moderately developed. It may progress rapidly and cause the early 
death of the child, or it may develop gradually or come to a stand- 
still. In the more marked forms of the disease the ventricles are 
widely diluted and filled with serum, which is usually transparent.* 
Not only the lateral ventricles, but also the third and fifth, may be 
involved ; the fourth is less apt to participate in the lesion, although 
it is sometimes dilated, as well as the central canal of the cord. 

The distention, especially of the lateral ventricles, may be so great 
that the brain tissue over the vertex is crowded up into a thin layer 
beneath the dura mater, or it may be entirely destroyed. When the 
dilatation of the ventricles is considerable, the convolutions are flat- 
tened (see Fig. 175) and may be almost entirely obliterated. The 
skull bones may be thin and bulging over the forehead and vertex ; 
the fontanelles and sutures widely open. The ependyma in these 
cases is usually thick and rough, but it may be softened, and the 



368 THE NERVOUS SYSTEM. 

blood vessels may be dilated. The basal portions of the brain may 
be flattened, but are usually much less affected than the upper por- 
tions. The brain tissue is usually soft and ansemic. 
. 2. Secondary Hydrocephalus. — This may occur in children and 
adults, and may be a result of epidemic cerebro-spinal meningitis, or 
of acute meningitis, or of chronic meningitis. It sometimes occurs 
in chronic alcoholic poisoning and in general paralysis of the insane. 
The amount of dilatation of the ventricles varies greatly in these 
cases, but it is never so great as in congenital hydrocephalus, and is 
not accompanied by the changes in the shape of the skull which 
form so prominent a feature in the latter disease, since the bones are 
firmer and the sutures united. In this form of chronic hydrocepha- 
lus the changes in the ependyma above described are usually more or 
less well marked, and they may be associated with the production of 
fibrin and pus. 

3. Primary Hydrocephalus in Adults. — The conditions leading 
to this form of lesion are not understood. It is apt to occur in persons 
over thirty years of age. Sometimes one, sometimes both lateral 
ventricles are dilated. The dilatation is usually moderate, sometimes 
very slight, and never as great as in congenital hydrocephalus. The 
ventricles usually contain transparent serum, and the ependyma is 
thickened and roughened. In some cases it is the only lesion found 
to account for the death of the patient. 



TUMORS. 

The new formation of connective tissue in the ependyma, al- 
though usually diffuse, may be circumscribed and form small, pro- 
jecting connective-tissue nodules, which may be reckoned among 
the fibromata. Small fibromata are sometimes detached from the 
walls of the ventricles and lie free in the cavity. Small lipomata, 
>angiomata, and also sarcomata and gliomata occur rarely. Chon- 
dromata and angiomata may occur in the choroid plexus, and the 
latter are sometimes as large as a hen's egg. The choroid plexus is 
not infrequently the seat of transparent cysts, usually of small size ; 
they may contain a clear fluid, or colloid material, or droplets of fat, 
or calcareous particles. A small dermoid cyst containing hairs has 
been described. These cysts have no special pathological signifi- 
cance. 

Primary carcinomata are sometimes found in the ventricles. 

The calcareous bodies called brain sand 1 occur frequently in the 
choroid plexus (see Fig. 162), and corpora amylacea may occur here 
and beneath the ependyma. 

1 The little, hard masses called brain sand consist of aggregations of small parti- 



THE NERVOUS SYSTEM. 369 

C^ysticercus and echinococcus cysts are sometimes found free in 
the fluid of the ventricles. 



PINEAL GLAND. 

This little body, about the size of a cherry stone, is composed of 
connective tissue enclosing cavities, which are filled with reticulated 
tissue and round cells. The cavities often contain brain sand. It 
is said * that the pineal gland is an aborted or rudimentary organ 
and may be related to a median eye of invertebrate type. 

A small number of tumors belonging to the class of teratoma 
have been described as originating in the pineal gland. 

Weigert 2 describes a tumor, about 3^- cm. in diameter, composed 
of epidermis, hair follicles, hair, sebaceous glands, cartilage, fat, 
smooth muscle, and cylindrical epithelium. 

Falkson* describes a chondro-cysto-sarcoma, 5.8 cm. in diameter, 
which apparently originated in the pineal gland. 

Turner 4 describes a tumor of the pineal gland, projecting into 
the third ventricle and the left lateral ventricle, of the size of a kid- 
ney. The tumor was composed of fusiform cells, of nerve ganglion 
cells, of tubules and acini lined with cylindrical epithelium, and of 
more irregular spaces filled with large polygonal cells. 

Coats 5 describes a tumor, three inches in diameter, growing into 
the third ventricle, the aqueduct of Sylvius, and the fourth ventricle. 
It was composed of fusiform cells, of tubules lined with cylindrical epi- 
thelium, of irregular masses of epithelium, of cartilage, and of smooth 
muscle. 

THE PITUITARY BODY. 

This structure, called the Hypophysis cerebri, consists of two lobes. 
The anterior lobe is composed of a connective-tissue stroma enclosing 
cavities which are packed full of nucleated cells of various sizes and 
shapes, some of them resembling nerve cells. The posterior lobe is 
composed of vascular connective tissue. 

Weigert e describes a tumor, as large as a hen's egg, which resem- 
bled in its structure the normal anterior lobe of the pituitary body, 
and which he regards as a hypertrophy of that body. 

cles of carbonate and phosphate of lime, with a very small amount of phosphate of 
ammonia and magnesia. With these there is more or less organic matter. 

1 Quarterly Jour, of Micr. Science, 1886. 

2 Virch. Arch., lxv., p. 212. 3 Ibid., lxxv., p. 550. 

4 Trans. Lond. Path. Soc, xxxvi. 5 Ibid., xxxviii. 

6 Virch. Arch., lxv., p. 219. 



370 THE NERVOUS SYSTEM. 

Weigert also describes a gummy tumor of the pituitary body as 
Large as a hazelnut. 

Weichselbaum describes an adenoma of the pituitary body, as 
large as a pigeon's egg, closely resembling the structure of the nor- 
mal anterior lobe of this body ; a small lipoma ; and a pituitary body 
with colloid cysts, lined with ciliated epithelium. 1 



THE BRAIN. 
THROMBOSIS AND EMBOLISM. 

In studying the occurrence and effects of thrombosis and embolism 
in the brain, certain peculiarities of the circulation should be borne 
in mind. The arteries of the brain are in part terminal arteries (see 
page 74), in part such as have anastomoses among their branches. 
Thus the arteries which are distributed to the cortical region form 
abundant anastomoses in the pia mater and are verv small when they 
enter the brain, while those which are distributed to the basal re- 
gion, and which supply the basal ganglia, are larger and do not, be- 
yond the circle of Willis, form anastomoses with one another. Thus 
it is that occlusions of the arteries supplying the basal ganglia are 
of much more serious import, aside from the importance of the parts 
involved, than those passing to the cortex. 

Thrombi may form in the arteries as a result of any degenerative 
or inflammatory process in the wall of the vessel leading to a rough- 
ening or death of its intima, or from pressure upon the vessel from 
without, or they may occur in vessels in whose walls we can detect 
no primary lesion. The most common causes are atheroma and 
simple endarteritis. Thrombi may also form around an embolus 
which does not entirely occlude the vessel. 

Emboli of the cerebral arteries most commonly arise from acute 
or chronic endocarditis or cardiac thrombi ; they may arise from 
aneurisms or atheroma of the aorta, from the carotid or vertebral 
arteries, or from the pulmonary veins. The materials constituting 
emboli vary greatly, depending on their mode of origin (see page 
73). The effects on the brain tissue of emboli and thrombi of the 
arteries are essentially the same in their main features. In some 
cases, however, in which large emboli, usually from endocarditis, 
suddenly block up a large vessel, the individual may die almost in- 
stantly without other apparent lesion than the stoppage of the vessel. 

In general, the first effect of the occlusion of an artery is to 

1 Consults. Hippel, Virchow's Arch., Bd. cxxvi., p. 124, 1891. 



THE NERVOUS SYSTEM. 



371 



deprive the region to which it is distributed of blood. In arteries 
whose branches anastomose, as in the cortex of the brain, the af- 
fected area is soon supplied with blood by the establishment of a col- 
lateral circulation. In terminal arteries, on the other hand, the 
blocking of the vessel is followed, as a rule, by degenerative changes 
and softening in the brain tissue, The appearances which these de- 
generated areas present vary greatly, depending upon the stage of 
the degeneration and the amount of blood which may be extra- 
vasated. Dense infiltrations of the brain tissue with blood, as in 
hsemorrhagic infarctions from emboli in other parts of the body, do 
not usually occur, although considerable blood may be extravasated. 




Fig. 176.— Degenerated Cells, Cholesterin Crystals, and Corpora amylacea from Brain 
Tissue in Embolic Softening. 

a, fatty ganglion cells: 6, corpora amylacea; c, cell containing very large number of fat drop- 
lets (compound granular or Gluge's corpuscles) ; d, cholesterin crystals. 



Areas of softening in which there is little extravasation of blood 
are usually white or yellow in color (ivhite or yellow softening). 
When much blood is present the process is frequently called red 
softening. The tissue in the affected area gradually softens and 
may become diffluent. Microscopically, the softened tissue is seen to 
consist of more or less fluid with broken-down brain tissue, frag- 
ments of nerve fibres, droplets of myelin, nerve cells, shreds of 
neuroglia tissue and blood vessels, and red and white blood cells. 
Then evidences of degeneration are seen in the presence of fat 



372 



THE NERVOUS SYSTEM. 



granules and droplets, larger and smaller cells densely crowded 
with droplets of fat (so-called G-luge's corpuscles or compound 
granular corpuscles) (see Fig. 176). Various kinds of cells and cell 
fragments, more or less granular and fatty, and also corpora amyla- 
cea, blood pigment, fat crystals, and cholesterin crystals, may be 
found. The walls of the blood vessels may also be in a condition of 
fatty degeneration (Fig. 177). The color of the softened mass will 
of course depend upon the relative amounts of these elements. 

The tissue may remain for a long time in the soft condition, or it 
may be absorbed and replaced by a connective-tissue cicatrix which 
may be more or less pigmented ; or a wall of connective tissue may 
form about it, converting it into a well-defined cyst, with or without 
pigmented walls ; or the mass may dry and form a dense, structure- 
less nodule. Acute inflammatory changes may occur about the 




Fig. ITT.— Blood Vessels from an Area op Embolic Softening of Brain. 
The walls of the vessels, particularly the endothelial cells, contain fat granules and fat droplets. 



dead tissue. In cases of infectious emboli numerous abscesses may 
be formed in addition to their mechanical action. 

Thrombi are most frequent in the internal carotids, less so in the 
middle cerebral, basilar, and vertebrals. They may occur, but still 
less frequently, in other cerebral arteries. Emboli are most common 
in the middle cerebral artery, next in the internal carotid, and then 
in the basilar. The relative frequency with which embolism occurs 
in the middle cerebral artery is attributable to the directness with 
which the blood passes into this artery from the heart. The great 
significance attaching to embolism of the middle cerebral artery is 
evident when we remember thr.t its branches are terminal arteries, 
and are distributed to such important structures as the lenticular and 
caudate nucleus, the internal capsule, and the optic thalamus. 



THE NERVOUS SYSTEM. 373 



HYPEREMIA AND ANAEMIA. 



The appearance of the brain tissue after death does not always 
furnish reliable indications of its blood contents during life, though 
they are perhaps more to be depended on than the appearance of the 
meninges. 

Some of the more common conditions determining hyperemia 
which are mentioned above as influencing the meninges apply also 
to the substance of the brain. In sections of hyperaemic brains the 
small blood points from the cut ends of small vessels are more nu- 
merous and conspicuous than under normal conditions, and the brain 
tissue, particularly the gray matter, may have a diffuse red color. 
If excessive the convolutions may be somewhat flattened, and the 
brain tissue and pia mater may be oedematous, and the ventricles con- 
tain fluid. The congestion of the vessels may be general or localized. 

Ancemia of the brain may be either local or general. It may de- 
pend upon a general anaemia or upon general disturbances of the 
circulation, such as mitral stenosis or regurgitation ; or upon local in- 
terference with the arterial blood supply, such as complete or partial 
obstruction of the arteries from thrombi, emboli, inflammatory 
changes, spasmodic contractions, etc., or from tumors, exudations, 
and blood extravasations pressing upon the vessels from without. 
In oedema of the meninges, and in the presence of internal hydro- 
cephalus, the brain tissue is apt to be anaemic. The brain tissue in 
anaemia looks whiter than usual, the contrast between the gray and 
white matter is less marked, and the small blood points usually seen 
on section from divided vessels may be very inconspicuous or almost 
entirely absent. 

CEDEMA 

of the brain tissue may accompany either general or localized hyper- 
aemia or it may accompany anaemia, and it seems in most cases, 
though not always, to be dependent upon conditions which induce 
these alterations in the blood contents of the brain. In some cases of 
marked impoverishment of the blood a so-called hydrcemic oedema of 
the brain is found. Very marked oedema of the brain may exist 
without any accompanying brain symptoms. On the other hand, 
persons may die comatose with no other gross lesion than oedema, 
either with or without oedema of the pia mater. This is seen with 
especial frequency in acute and chronic alcohol poisoning, but may 
occur under other conditions. A careful microscopical examination 
of the brain under these conditions will frequently reveal structural 
lesions of far more serious import than the oedema. 

Under the designation of "serous apoplexy," oedema of the. brain 
was formerly considered of importance, in the absence of other le- 



374 THE NERVOUS SYSTEM. 

sions, as a cause of death. But the accumulation of knowledge on 
this subject has led to the general belief that simple cerebral oedema 
as an independent condition has not the significance formerly as- 
cribed to it, and it should be accepted, if ever, with great reserve as 
a cause of death. 

HEMORRHAGE. 

Haemorrhages in the substance of the brain may be very small 
and punctate, and are then usually called capillary haemorrhages; 
or they may result in the collection in the brain tissue of masses of 
blood of considerable size, which are called apoplectic foci or clots. 
These forms of haemorrhage may be associated, or a number of 
capillary haemorrhages may join to form an extensive clot. 

Capillary haemorrhages may look, on section of the brain, like 
the severed ends of hyperaemic blood vessels, or the tissue about them 
may be more or less tinged with blood. Microscopically, the peri- 
vascular spaces will be found distended with blood, which may have 
escaped into them and more or less broken down the brain tissue. 
They may occur singly, but are frequently multiple, so that the brain 
tissue is besprinkled with blood points. Degeneration of the extra- 
vasated blood may give rise in later stages to reddish or brown or 
yellowish circumscribed discoloration of the brain tissue, due to gran- 
ules and crystals of blood pigment intermingled with broken-down 
brain tissue, with more or less fatty degeneration of its elements. 
Capillary haemorrhages may be due to fatty degeneration of the ves- 
sels leading to rupture ; or the extravasation may be due to diape- 
desis, or it may depend upon conditions which we do not understand. 
They frequently occur in the vicinity of apoplectic clots and tumors , 
they may be due to thrombosis of the veins or of the sinuses of the 
dura mater ; they not infrequently occur in acute encephalitis, in 
congestive hyperaemia, in acute mania, and in delirium tremens ; 
and they may be associated with general diseases, such as scurvy, 
purpura haemorrhagica, typhus fever, pyaemia, ulcerative endocar- 
ditis, etc. ; they may be associated with embolic softening. 

Apoplectic foci may result from the coalescence of numerous 
capillary haemorrhages ; from injury, or from rupture of diseased ar- 
teries, either with or without changes in the blood pressure. Haem- 
orrhages from injury to the skull may occur as well without as with 
fracture, and may be situated over the vertex as well as at the base 
of the brain, and vary in extent and seat, depending upon the cha- 
racter and point of the injury and the size of the vessels involved. 
The so-called spontaneous haemorrhages, other than those of capil- 
lary origin, which give rise to masses of blood and broken-down 
brain tissue, may vary in size from that of a pea to those occupying 



THE NERVOUS SYSTEM. - 375 

a large part of a hemisphere. They are due, in a very considerable 
proportion of cases, to the rupture of small arterial aneurisms, but 
may arise from weakening of the walls of the arteries, from arteri- 
tis, atheroma, or fatty degeneration. These latter forms of disease 
doubtless give rise in most cases to the formation of the aneurisms 
whose rupture is in so many cases the immediate cause of the haem- 
orrhage. Aneurisms of the cerebral arteries may be as large as a 
pea or hazelnut, but those most frequently met with and causing 
apoplexy are usually small — called miliary aneurisms — and may be 
microscopic in size, varying from this up to that of a large pin's 
head or larger. They may be sacculate or fusiform, and frequently 
exist in considerable numbers. They may occur in any of the small 
arteries of the brain, but are said to be most frequent on the branch ■ 
es of the middle cerebral artery. It is asserted that the bursting 
of miliary aneurisms is the nearly if not quite exclusive cause of the 
formation of spontaneous apoplectic clots, but this we do not be- 
lieve to be true. As to the immediate cause of rupture, either of 
aneurisms or otherwise diseased blood vessels in the brain, we are in 
many cases entirely ignorant. In some cases it seems to be due to 
an increased arterial tension in such diseases of the heart as induce 
this change, as in the cardiac hypertrophy which may accompany 
some forms of chronic diffuse nephritis ; or it may result from un- 
usual exertion or mental excitement ; but, as above stated, in many 
cases the immediate inciting cause is not evident. 

The most frequent seat of haemorrhage is in the corpora striata 
and optic thalami, and the brain tissue in their vicinity, and here 
they occur most often in the parts supplied by the branches of 
the middle cerebral artery. The possibility of haemorrhage in the 
floor of the fourth ventricle as a cause of sudden death should be 
borne in mind in investigating cases of sudden death from obscure 
causes. 

Haemorrhages frequently seriously affect other portions of the 
brain than those immediately supplied by the ruptured vessels. 
Thus haemorrhages in the cortical substance or beneath the pia mater 
may force their way deep into the brain substance ; or, in haemor- 
rhage in the brain substance, the blood may burst into the ventricles 
or work its way into the intermeningeal space, and, either at the seat 
of its occurrence or in the situations into which it is forced, it may 
give rise to serious compression of the brain. Portions of the brain 
containing large extravasations may be enlarged, the tissue anaemic 
from pressure, the convolutions flattened, and the surface dry. As 
the blood is poured out the brain tissue is usually torn and lacerated, 
so that the apoplectic clot usually consists of detritus of brain tissue 
intermingled with blood. If, however, the blood is poured out from 



376 THE NERVOUS SYSTEM. 

a single vessel, the lacerated brain tissue may be pressed aside, and 
the greater portion of the red mass may consist of pure blood clot. 

The appearances presented by haemorrhages in the brain vary 
greatly, depending upon the time which has elapsed since their occur- 
rence. If life continue, the oedema which usually soon occurs in the 
vicinity of the haemorrhage disappears and the clot becomes drier 
and firmer ; gradually the blood undergoes the usual series of 
changes seen in extravasation : the haemoglobin decomposes, form- 
ing granules and crystals of blood pigment : the blood cells and 
fibrin undergo degeneration and absorption; the detritus of brain 
tissue undergoes fatty degeneration. As these alterations occur the 
color changes to reddish-brown, orange, or yellow, and the adjacent 
brain tissue may be discolored by imbibition. 

Inflammatory reaction may occur in the vicinity, leading either 
to the formation of a more or less pigmented cicatrix, or to a cyst 
with yellowish fluid contents and a fibrous, more or less pigmented 
wall. The process of degeneration and absorption of the blood and 
broken-down brain tissue, and their replacement by a cyst or by a 
cicatrix, is a slow one, and the cysts and cicatrices may resemble those 
formed at the seat of embolic softening. Not infrequently we find in 
the brain of a person dead from recent apoplexy the remains of old 
clots presenting some one of the above-described stages of absorption. 
The apoplectic cysts and cicatrices persist for a long time after their 
formation. 

CHANGES IN THE GANGLION CELLS IN TOXEMIA. 

There is much reason for believing that in many of the acute in- 
fectious diseases, particularly in those which are characterized by the 
wide distribution of toxic agents in the blood from some special 
seat of microbic growth, there may be important and often profound 
changes in the ganglion cells of the central nervous system, some of 
which are associated with marked structural alterations in the cyto- 
plasm. Such changes have been already demonstrated in hydro- 
phobia and in tetanus as well as in local inflammatory and destruc- 
tive lesions in the spinal cord. These changes may be looked upon, 
at least for the present, as the analogues of the degenerative changes 
which are more familiar in the parenchyma cells of such viscera as the 
liver, kidney, etc., and like them may vary greatly in degree and 
significance. The whole subject of ganglion-cell changes in toxaemia 
offers a most promising field for research. 

The chromophylic masses in the ganglion cells ma}', under the 
influence of various poisons and other deleterious agencies, disin- 
tegrate or largely disappear, being finally represented only by fine 
granules scattered through the cytoplasm or gathered in masses 01 



THE NERVOUS SYSTEM. 



377 



about the periphery. The nucleus may undergo various degrees of 
disintegration or may entirely disappear (see Fig. 178). 

Various degrees of pigmentation may be associated with these 
changes in the cell. 

These finer alterations in the ganglion may be demonstrated by 
the use of Nissl's stain (see page 412). 

It is important to recognize the possibility of serious structural 
changes in the nervous system as the result of the action of toxic 
agents of microbic origin, but also as the result of so-called " auto- 
intoxication," from the presence in the body of excrementitious 
substances which have failed of proper elimination. 

But great care is necessary not only in the technical procedures 
to which these delicate structures must be subjected, but also in the 






Fig. 178.— Ganglion Cells op the Spinal Cord. 
Stained by Nissl's method with methylene blue. Showing, A, normal ganglion cells; B, gan- 
glion cells in acute myelitis with marked changes in the chromophylic masses of the cell bodies. 

interpretation of appearances in a field in which "the morphological 
norm has been as yet so inadequately investigated and in which 
nutritional and functional changes are still so obscure. 1 



SECONDARY DEGENERATIONS. 

Lesions of the brain which involve the destruction of motor gan- 

1 An interesting consideration of the relation of infectious processes to diseases 
of the nervous system, by Putnam, may be found in the American Journal of the 
Medical Sciences, March, 1895. 

For a resume of the recent observations on the degenerative and regenerative proc- 
esses in the nervous system, with bibliography, consult Stroebe, Centralbl. f. allg. 
Path, und Path. Anat., December 15th, 1895. Consult also Berkley, Medical Record, 
March 7th, 1896. 
31 



378 THE NERVOUS SYSTEM. 

gliou cells or nerve fibres are regularly followed after a time by de- 
generative changes in these nerve fibres below the seat of lesion. It 
is particularly lesions in the central convolutions, the internal cap- 
sule, portions of the corona radiata, and the pes pedunculi, which 
destroy the motor fibres passing through these parts, and are followed 
by degenerative changes in the fibres below. The most important 
and frequent lesions followed by this effect are those involving the 
anterior two-thirds or three-fourths of the internal capsule. It will 
suffice merely to mention these changes here, as they are considered 
more in detail in the section devoted to lesions of the spinal cord 
(page 393). 

HYPERTROPHY AND ATROPHY OP THE BRAIN. 

True Hypertrophy of the brain is rare, and probably always con- 
genital. An increase in the size of the brain from the proliferation 
of the neuroglia sometimes occurs in children either before or after 
birth, less frequently in youth, and very seldom in adults. The 
white substance of the hemispheres is increased in amount. If it 
take place before the ossification of the cranium, the bones are sep- 
arated at the sutures and f ontanelles ; if after this, the inner table of 
the skull may be eroded and thinned. When the cranium is opened 
the dura mater appears tense and anaemic, the convolutions of the 
brain are flattened, the brain substance is firm and anaemic, the ven- 
tricles are small, the ganglia and cerebellum are either of normal size 
or compressed. 

The disease is usually very chronic, and destroys life with symp- 
toms of compression of the brain. There may, however, be acute 
exacerbations. 

Atrophy, — This may occur as a senile change, or, in adults, in 
chronic alcohol, opium, or lead poisoning, in chronic insanity, and in 
chronic meningitis or from local interference with the circulation. 
In children who are much reduced by chronic diseases atrophy of the 
brain may accompany atrophy of the rest of the body. 

The atrophy affects principally the cerebral hemispheres, and may 
be uniform or more marked in some parts than in others, involving 
the whole of a hemisphere or of a lobe or only single convolutions or 
groups of these (Fig. 179). The convolutions are small, the sulci 
broad, the ventricles usually dilated, the brain tissue firm, the gray 
matter discolored, the white substance grayish in color; the blood 
vessels may be dilated. The basal ganglia may be small. Serum 
accumulates in the pia mater and the ventricles; the pia mater, and 
often the skull, become thickened; the brain tissue may be cedema- 
tous or contain small haemorrhages. The nerve elements of the brain 



THE NERVOUS SYSTEM. 3T9 

tissue are those most involved in the atrophy, the diminished areas 
being usually harder and firmer than normal. 

WOUNDS OF THE BRAIN. 

The brain may be directly wounded by a foreign body, or indi- 
rectly by fragments of bone driven into it, or it may be lacerated by 
severe contusion without fracture or solution of continuity of the 
skull. It is very difficult to estimate the degree of injury which 
must cause death, since persons frequently die from slight, and may 




Fig. 179.— Atrophy of a Circumscribed Portion of Brain Convolutions in a Child. 
From a lesion of the corresponding blood vessels. (From a specimen loaned by Dr. Freeman.^ 

recover from very severe, wounds of the Brain. In incised wounds of 
the brain more or less haemorrhage occurs at the seat of lesion, and 
the brain tissue in the vicinity soon undergoes degenerative changes. 
These may be comparatively slight or extensive. Inflammatory re- 
action may occur in the vicinity, and the adjacent brain tissue, as 
well as the hemorrhagic and degenerated area, become infiltrated 
with pus cells. After a time the injured and degenerated area may 
become surrounded by new-formed connective tissue, and the de- 
composed extravasated blood and detritus of brain tissue, more or 
less fatty, may be absorbed, and thus after a time the part heals by 



380 THE NERVOUS SYSTEM. 

a more or less pigmented cicatrix. The healing is in most cases very 
slow and may occupy months or even years. The pia mater may 
participate to a marked degree in the inflammatory healing process. 
Abscesses may form near the seat of injury. 

After wounds which involve the removal of portions of the cra- 
nial bones, it is not uncommon after a few days to see a bleeding 
fungous mass project through the opening. This mass, some- 
times wrongly called hernia cerebri, consists of degenerated brain 
tissue, blood, and granulation tissue, with more or less pus. The 
brain tissue below it is degenerated, broken down, soft, and puru- 
lent, and there is often abscess in the adjacent brain tissue. Such 
wounds may finally heal by the absorption of the broken-down brain 
tissue and blood, and its substitution by granulation tissue. 

Lacerations of the brain tissue without fracture may appear 
shortly after the injury as simple more or less circumscribed areas 
of capillary haemorrhage ; the brain tissue about these may degene- 
rate, pus may form, and abscesses be developed ; or the degenerated 
and lacerated tissue may be gradually replaced by granulation tis- 
sue which finally forms a cicatrix. The process of degeneration 
and softening and of healing in such lacerations of brain tissue may 
occur very slowly indeed, even occupying years, and not infre- 
quently the degenerative changes are very extensive and progres- 
sive. In many cases, of course, the injury is so extensive, or in- 
volves such important parts of the organ, that very little or no 
inflammatory or degenerative change takes place before death. 

HOLES OR CYSTS IN THE BRAIN (PORENCEPHALUS). 

Larger and smaller holes may be found in the brain tissue from 
dilatation of the perivascular lymph spaces, or well-formed cysts 
may exist from haemorrhage, inflammatory softening, hydatids, etc. 
There are, however, cases in which one or several holes of varying 
size are found in the brain which cannot be determined to have 
either of the above modes of origin. They may lie deep in the brain 
substance or close under the pia mater, or may communicate with 
the ventricles. This condition is sometimes called porencephalic, 
and may co-exist with various mental aberrations, hydrocephalus, etc. x 

INFLAMMATION OF THE BRAIN (ENCEPHALITIS). 

It has been already mentioned that the brain tissue about haemor- 
rhages and areas of embolic and thrombotic softening may undergo 

1 Consult v. Kahlden, "Ueber Porencephalic, " Ziegler's Beitr. zur Path. Anat., 
etc., Bd. xviii., p. 231. 



THE NERVOUS SYSTEM. 381 

inflammatory changes leading to the formation of new connective 
tissue. There is a class of cases in which localized areas of the brain 
undergo softening, with more or less extravasation of red and white 
blood cells and hyperemia of the blood vessels, so that the softened 
material consists, as seen under the microscope, of detritus of brain 
tissue in a condition of fatty degeneration, with more or less pus 
cells or pigment. When such areas are red in color from inter- 
mingled blood cells or pigment the condition is called red inflam- 
matory softening. When fatty degeneration prevails, and the red 
blood cells or their derivatives are not abundant, the softened area 
looks yellow or yellowish- white, and this is often called yellow in- 
flammatory softening. The origin of these processes is very ob- 
scure and their inflammatory nature not well defined. 

Abscess of the Brain. — The small multiple abscesses of the brain 
which occur with pysemia form part of that disease and require no 
separate description. 

The large single abscesses occurring under different conditions 
are those to which the name of "abscess of the brain "is usually 
applied. 
- These abscesses occur in two forms : 

The non-capsulated abscess, an irregular cavity containing thin 
pus and softened brain tissue. The walls of the cavity are ragged 
and infiltrated with pus, and outside of the walls is a zone of cede- 
matous and softened brain tissue. If the abscess is near the pia ma- 
ter it may set up a meningitis ; if it is near the lateral ventricles it 
may rupture into them ; if it is near the sinuses of the dura mater it 
may cause thrombosis. 

The encapsulated abscess has a capsule of connective tissue, and 
contains thin or cheesy pus. 

Abscesses of the brain are usually single : they may attain a con- 
siderable size. They are most frequent in the cerebral and cere- 
bellar hemispheres, rare in the central ganglia, the pons, and the 
medulla oblongata. 

The most common cause of this disease seems to be chronic sup- 
purative otitis (42.5 per cent, Gowers), while acute otitis is a com- 
paratively rare cause. With the otitis there may also be caries of 
the temporal bone, suppuration of the mastoid cells, and inflamma- 
tion of the dura mater. The abscess is usually situated deep in the 
brain ; only rarely is it continuous with the inflamed dura mater and 
bone. When the abscess is deeply situated, and the bone and dura 
mater are not diseased, it is difficult to tell how the infection travels 
from the ear to the brain. Abscesses due to this cause are situated 
in the temporo-sphenoidal, the frontal, the occipital, and the parie- 
tal lobes, or in the cerebellum. 



382 THE NERVOUS SYSTEM. 

Another frequent cause of abscess of the brain is traumatism — 
blows or falls on the head (24 per cent, Gowers). Such injuries may 
not hurt the skull, or may produce fractures or necrosis. There is 
often a considerable interval between the time when the injury is 
inflicted and that when the symptoms of the abscess are developed. 

When the cranial bones are uninjured the abscess is situated deep 
in the brain ; when there is necrosis of the bones the abscess may 
be superficial ; when the bones are fractured the abscess may be 
either superficial or deep. The abscess is regularly situated beneath 
the point of injury, rarely in the opposite side of the brain. 

Chronic disease of the nose, either the mucous membrane or the 
bones, has been the cause of a few abscesses in the frontal lobes. 
Disease of the orbit has also given rise to abscesses in the same 
position. In a few cases the abscesses have been due to caries of 
various portions of the cranial bones. 

In a considerable number of cases (one-sixth, Gowers) no cause 
for the abscess has been discovered. 

Very frequently in acute meningitis there is an infiltration of pus 
cells along the walls of the vessels which enter the brain from the 
pia mater ; and under a variety of conditions which we do not un- 
derstand, as in some cases of typhoid fever, delirium tremens, ery- 
sipelas, and under many other conditions, there are numerous and 
sometimes very large numbers of leucocytes scattered through the 
substance of the brain, sometimes around the ganglion cells, some- 
times along the vessels in the perivascular sheaths. 

Chronic Interstitial Encephalitis — Sclerosis. — This lesion of 
the brain tissue may occur diffusely, occupying an entire lobe or 
more or less of the whole brain, or in circumscribed small areas. It 
consists essentially in an increase of the connective-tissue elements, 
the neuroglia, and an atrophy of the nerve elements, particularly the 
ganglion cells and the medullary sheaths of the nerves. With these 
changes are usually associated the formation of Gluge's corpuscles, 
corpora amylacea, granular and fatty degeneration of the nerve ele- 
ments, and thickening and proliferation of cells of the walls of the 
blood vessels. The areas of sclerosis may be very dense and hard, 
or gelatinous in consistence. 

The diffuse form of sclerosis is most frequently seen in general 
paresis of the insane, and not infrequently in the brains of drunk- 
ards. 

The circumscribed form of sclerosis, multiple sclerosis {sclerose 
en plaque), is much more common than the diffuse form, and may 
occur in the brain alone, or may be associated with a similar lesion 
in the spinal cord. It is almost entirely confined to the medullary 
substance, and the areas of sclerosis vary in size from that of a pea 



THE NERVOUS SYSTEM. 



3S3 



to that of an almond. They may be few or numerous, they may be 
white, grayish, or grayish-red m color, and are usually, but not 
always, sharply outlined against the unaltered brain tissue. Al- 
though in many cases the increase in the connective-tissue elements 
seems to be the primary lesion, and the degeneration of the nerve 
elements secondary to this, it is quite possible that in some cases the 
increase in connective tissue may be secondary to a degeneration of 
the nerve elements from loss of nutrition or from other causes. 



M 



M 



M 



, 







- 

3 



gfe 




/X 



Fig. 180.— Syphilitic Obliterating Entjarterltis of a Cerebral Artery, x 50 and reduced. 

There is reason for the belief that multiple sclerosis may be the re- 
sult of disseminated local necrotic lesions of acute infectious diseases 
— scarlatina, for example — occurring at an early period of life. 1 

Encephalitis in the New-born. — This condition, first described 
by Yirchow, is said to consist in the formation of circumscribed col- 
lections of cells of various sizes containing many fat granules (granu- 
lar corpuscles) and forming yellowish masses, from 1 mm. to 6 mm. 



See Oppniheim, Berl. klin. AVochenschrift, March 2d, 189G. 



384 



THE NERVOUS SYSTEM. 



in diameter, in the brain tissue. A more diffuse occurrence of granu- 
lar corpuscles is also described, but this is said by some observers to 
be physiological. The nature of this lesion is but little understood 
and is still the subject of controversy. 

Syphilitic Inflammation of the Brain sometimes results in the 
formation of so-called gummy tumors. These are most frequently 
found near the periphery of the brain, not infrequently connected 
with the meninges, and may be sharply circumscribed. The central 
portion of the tumor is usually in a condition of cheesy degeneration, 
and in the periphery we see fibrous tissue or a dense infiltration of 
small spheroidal cells. 

Syphilitic inflammation of the brain very frequently occurs in 
a diffuse form, characterized by the formation of a gelatinous, grayish 




• - ? 



■&.; 






Fig. 181.— Solitary Tubercle op Cerebellum. 
a, a, miliary tubercles with giant cells; b, 6, miliary tubercles without giant cells; c, diffuse 
tubercle tissue; d, central cheesy mass; e, nerve tissue of the cerebellum. 

tissue consisting of a more or less homogeneous or granular base- 
ment substance, with numerous small spheroidal cells. The nerve 
elements are atrophied. Obliterating endarteritis may occur as a re- 
sult of syphilitic poisoning (Fig. 180). 

Tuberculous Inflammation of the brain substance usually mani- 
fests itself in the formation of circumscribed masses of new tissue 



THE NERVOUS SYSTEM. 385 

from 0.5 cm. to 1 cm. in diameter, or larger. These may be single 
or multiple, are most common in young persons, and very fre- 
quently occur in the cerebellum. They are apt to occur in connec- 
tion with tuberculous inflammation of other organs. They are fre- 
quently called solitary tubercles, and usually consist of a dense 
central cheesy mass, around which is a grayish zone containing 
tubercle granula, numerous small spheroidal cells, with occasionally 
larger polyhedral cells and giant cells (Fig. 181). They do not, as 
a rule, seem to be formed by an aggregation of miliary tubercles, 
although these may be present in the periphery. Tubercle bacilli 
have been found in these solitary tubercles. 

They sometimes suppurate and break down, and then may simu- 
late simple abscesses. 

Conglomerate and scattered miliary tubercles of the ordinary 
form sometimes occur in the brain, usually in connection with tuber- 
cular inflammation of the meninges or ependyma. 

LESIONS OF THE BRAIN IN GENERAL PARESIS OF THE INSANE. 

The changes in this disease are in the main those of chronic dif- 
fuse encephalitis, but the appearances vary greatly and depend to 
some extent upon whether the brain is examined in early or late 
stages of the disease. According to Meyer, in the early stages of the 
disease the convolutions, particularly of the anterior cerebral lobes, 
are swollen, the gray matter congested and softened in places. The 
brain tissue is more or less infiltrated with leucocytes. Fatty de- 
generation of the walls of the capillaries, and punctate haemorrhages, 
are also common. 

In later stages of the disease a great variety of changes may be 
observed : hemorrhagic pachymeningitis, thickening of the dura 
mater, and close adhesions to the skull ; thickening and opacities of 
the pia mater, adhesions of the latter to the dura mater and to the 
brain tissue. The brain tissue is apt to be atrophied, and the ventri- 
cles dilated and filled with fluid. The pia mater may be cedematous, 
the ependyma thickened and roughened. On microscopical exami- 
nation the neuroglia is found to be increased in amount, the ganglion 
cells shrunken and sometimes pigmented ; the nerve fibres may also 
be atrophied, and the blood vessels in a condition of fatty or hyalin 
degeneration. There may be an accumulation of fatty and granular 
cells along the walls of the blood vessels. Secondary degenerations 
in the spinal cord are not infrequently observed. 

It is very difficult to make positive and definite statements regard- 
ing many such lesions of the brain as those just indicated, or in 
general of brain lesions whose nature must be revealed by microsco- 
pical study, because our technical procedures in the study of the 



386 • THE NERVOUS SYSTEM. 

brain, even in normal conditions, are still quite unsatisfactory and 
incomplete. The brain tissue is so delicate and liable to post-mortem 
changes, and the effects of different preservative agents are so liable 
to variations, that great caution is necessary in arriving at conclu- 
sions regarding the minuter lesions affecting the nerve tissue of the 
brain. 

PIGMENTATION. 

This may occur in any portion of the brain or its meninges from 
the decomposition of extravasated blood. In persons affected by 
malaria the gray matter of the brain has sometimes an unusually 
dark or even blackish appearance. This color is due to the presence 
of black pigment granules within the capillary blood vessels. The 
obstruction to the vessels by masses of these pigment granules may 
cause capillary apoplexies. The pigment may also be found in the 
walls and in the lumina of the vessels of the pia mater. 

Pigmented patches of congenital origin are not infrequently seen 
in the pia mater. They may be due to the presence of branching 
pigmented cells. 

TUMORS OF THE BRAIN. 

Neuroglioma ganglionare. — This is a form of tumor probably 
due to disturbances in the development of the brain. It occurs in 
the form of circumscribed tumors or of diffuse enlargements of por- 
tions of the brain. The pia mater over these tumors is unchanged 
and the convolutions retain their shape. The tumors are formed of 
neuroglia, in which are contained little groups of ganglion cells 
(Ziegler). 

Glioma. — This is the most common tumor of the brain. It occurs 
with especial frequency in children and young adults. Such tumors 
occur in all parts of the brain, but they are found most frequently in 
the cerebrum. There may be a single tumor, or there may be sev- 
eral such tumors in different parts of the brain ; some of them attain 
a large size. These tumors may be sharply circumscribed, or merge 
imperceptibly into the brain substance ; sometimes the tumor is ar- 
ranged so as to form the wall of a cyst which contains clear serum. 
They may be white and hard ; gray, soft, and gelatinous ; infiltrat- 
ed with small haemorrhages ; or partly degenerated and softened. 
The brain tissue around these tumors may be inflamed or necrotic. 
The tumors are composed of neuroglia, the relative quantity of neu- 
roglia cells (Fig. 137) and of fibrils (Fig. 136) varying in the different 
tumors. 

If the cells are very numerous, with but little basement sub- 
stance, the tumor is called a glio-sarcoma. 



THE NERVOUS SYSTEM. i f 

Sarcomata occur in any part of the brain. They are single cr 
multiple. They are composed of round or fusiform cells with more 
or less basement substance. 

Endotheliomata are found in the substance of the brain. They 
are of the same types as have been described as occurring in the 
pia mater. 

Myxoma, fibroma, lipoma, and osteoma are rare forms of brain 
tumor. 

Angioma. — Small collections of dilated vessels are found in the 
substance of the brain. They seem to be congenital, like the nsevi 
of the skin. 

The cysts of the cerebellum are very curious bodies. They are 
found in young persons and in adults. They occur in any one of the 
lobes of the cerebellum. They may be as large as a hen's egg. They 
contain clear serum or colloid matter, and their walls are formed of 
thickened neuroglia. We are ignorant of their mode of origin. 
They give marked clinical symptoms and are regularly fatal. 

PARASITES. 

Cysticercus and, more rarely, echinococci are found in the brain. 

' MALFORMATIONS. 

Cyclopia. — This malformation consists in an arrest of develop- 
ment affecting the cerebrum, which, instead of separating into two 
hemispheres, remains single, with one ventricle, and the rudiments 
of the eyes usually become joined and form one eye. This single 
eye is in the middle of the face, near the place of the root of the 
nose, in a single orbit. Over this is an irregular body representing 
the nose. The rest of the face is well formed. Or the eyeball may 
be wanting entirely, or there are two eyes joined together, or, more 
seldom, two separate eyes. The orbit is surrounded by rudiments 
of four eyelids. The frontal bone is single, the nasal bones unde- 
veloped ; the ethmoid, vomer, and turbinated bones are absent. The 
optic nerve is double, single, or absent. There may be hydrocepha- 
lus. Such children are incapable of prolonged existence. 

Anencephalia. — This malformation may be of various degrees. 
The brain may be entirely absent, and the base of the cranium is 
covered with a thick membrane, into which the nerves pass. Or the 
membranes may form a sort of cyst containing blood and serum, or 
portions of brain. Of the cranial bones, only those which form the 
base of the skull are present (Acrania). The scalp is usually partly 
or entirely absent over the opening in the skull ; the eyes stand 
prominently out, and the forehead slopes sharply backward. This 
malformation may occur in otherwise well-developed children. 



388 THE NERVOUS SYSTEM. 

Hydrocephalus. — This lesion has been already considered on page 
367. It is probable that in some cases hydrocephalus intemus is due 
to a primary partial anencephalia, and that the accumulation of 
fluid is of secondary occurrence. In rare cases, only part of one lateral 
ventricle is hydrocephalic, giving to the head a protuberance on one 
side. The viability of the foetus depends upon the degree of the 
hydrocephalus. Hydrocephalus externus is an accumulation of 
serum beneath the pia mater, or, according to some authors, between 
the pia and dura mater. It causes dilatation of the cranium and 
compression of the brain. It is of very rare occurrence, and may 
also be secondary to partial anencephalia. 

Cephalocele, or Brain Hernia. — When abnormal openings exist 
in the skull from malformation, the contents of the cerebral cavity 
are apt to protrude in the form of larger or smaller sacs. This may 
occur in cases of well-marked anencephalia or in cases in which the 
brain is well developed. The protruding sac formed of the meninges 
may or may not be covered with skin. If the contents of the sac 
are simply fluid, the lesion is called hydromeningocele ; if composed 
of brain substance, encephalocele ; if the sac contain both fluid and 
brain substance, it is called hijdr encephalocele. The sacs may be 
very small or as large as a child's head. They may protrude from 
the top of the skull in acrania. They most frequently protrude 
through openings in the occipital bone, often hanging down in large 
sacs upon the neck ; also at the root of the nose, along the line of the 
sutures, at the base of the skull, and elsewhere. 

Microcephalia. — This is an abnormally small size of the brain, 
with a correspondingly small cranium. The diminution in size af- 
fects principally the cerebral hemispheres, though the other parts of 
the brain are also small. The convolutions are few and simple, the 
cavities often dilated with serum ; on the membranes there may be 
traces of inflammation. The cranium is small, the face large, the 
rest of the body small. The malformation is ir some cases caused 
by inflammation or dropsy of the brain during foetal life. It is en- 
demic in some countries, but single cases may occur anywhere. The 
foetus is viable. Absence or incomplete development of portions of 
the brain may occur, not only in idiots, but in persons whose minds 
are perfect. 1 

1 For a general consideration of malformations of the central nervous system con- 
sult Thoma, "Text-Book of Pathological Anatomy, " vol. i., p. 206 et seq. 



THE SPIRAL COED. 



THE MEMBRANES OF THE SPINAL COED. 

A.-THE DURA MATER SPINALIS. 

The dura mater spinalis, unlike that of the brain, does not serve 
as periosteum to the bones forming the cavity, so that the lesions 
of the two membranes differ somewhat. 



HEMORRHAGE. 

Haemorrhage may occur, as the result of injury, between the dura 
mater and periosteum, or it may occur in tetanus, as a result of circu- 
latory changes induced by muscular spasm, or in the asphyxia of 
new-born children. Small haemorrhages on the surfaces of the mem- 
brane may occur as the result of inflammation. 

Serous fluid may accumulate outside of the dura mater as a re- 
sult of post-mortem changes, or in connection with circulatory or 
inflammatory changes in the membranes. 

INFLAMMATION. 

Acute external pachymeningitis is usually secondary to dis- 
ease or injury of the spinal column, and may result in collections 
of pus between the dura mater and periosteum, usually most abun- 
dant posteriorly. Hcemorrhagic pachymeningitis occurs in the 
dura mater spinalis, with the formation of products similar to those 
observed in the brain, in the chronic insane and in drunkards. Sim- 
ple chronic pachymeningitis interna, with the formation of new 
connective tissue containing brain sand, is not infrequent. The 
new tissue may form minute projections or roughness of the sur- 
face, or, when more abundant, the psammomata. Tuberculr in- 
flammation of the dura mater spinalis may occur in connection with 
tubercular meningitis, or be secondary to tubercular inflammation 
of the vertebrae. 



390 THE SPINAL CORD. 



TUMORS. 



Fibromata, lipomata, cho?idromata, myxomata, endothe- 
liomata, and adeno-sarcomata 1 occur in the dura mater spinalis 
as primary tumors. Carcinomata and sarcomata may occur as 
secondary tumors. Small plates of new-formed bone are rarely 
found in the dura mater spinalis. 

PARASITES. 

Echinococcus developing outside of the spinal canal may perfo- 
rate the dura mater ; or the cysts may lie between the dura mater 
and the pia mater. 

It is obvious that even small tumors in the spinal canal may give 
rise to serious results from compression. 



B.— THE PIA. MATER SPINALIS. 

It is almost impossible in most cases in the pia mater, as well as' 
in the dura mater spinalis and in the spinal cord, to judge with cer- 
tainty, from the appearances after death of the blood contents of the 
vessels, of these parts during life. The same is true of abnormal 
quantities of serum found after death. The veins of the pia mater, 
especially in the posterior region, may be greatly distended with 
blood after death, without pre-existing disease ; and the intermen- 
ingeal space may contain much fluid under the same condition. 

HEMORRHAGE. 

Haemorrhages may occur from injury in connection with severe 
convulsions, or general diseases such as the hemorrhagic diathesis, 
scurvy, small-pox, etc. The haemorrhages under these conditions, 
except from injury, are not usually extensive. But in some cases 
of injury or cerebral apoplexy ; from the bursting of aneurisms of 
the basilar or vertebral arteries ; or in cases in which we cannot find 
a cause, a very large quantity of blood may collect between the dura 
and pia mater, and in the meshes of or beneath the latter. 

INFLAMMATION. 

Acute exudative spinal meningitis occurs under essentially the 
same conditions and with essentially the same post-mortem ap- 
pearances as acute cerebral meningitis, though it is less frequent. 
The exudations are apt to be most abundant in the posterior por- 
tions. It may be associated with a similar inflammation of the pia 

1 Hodenpyl, American Journal of the Medical Sciences, March, 1888. 



THE SPINAL CORD. 6 l 3l 

mater cerebralis, and the inner surface of the dura mater may be 
involved. The disease may be circumscribed, but usually affects 
the entire length of the membrane. 

Tuberculous inflammation is usually most marked, when asso- 
ciated with a similar condition of the pia mater cerebralis, in the up- 
per portions of the cord ; but it may extend over the entire membrane. 
The conditions under which it occurs and the character of the le- 
sions are similar in both. Chronic spinal meningitis is not infre- 
quent, manifesting itself in the formation of larger or smaller 
patches of new connective tissue or thickenings of the pia mater. 
The pia and dura mater may thus be firmly united in places by ad- 
hesions, or the pia mater may become closely adherent to the sub- 
stance of the cord. 

Not very infrequently large numbers of pigment cells are found 
in the pia mater spinalis, sometimes giving it a distinct gray or 
blackish color. 

TUMORS. 

Small plates of cartilage and bone are sometimes found in the 
pia mater. 

Fibromata, myxomata, sarcomata, and endotheliomata have 
been found. 

PARASITES. 

Cysticercus sometimes occurs in the meshes of the pia mater. 
THE SPINAL COED. 

HAEMORRHAGE. 

This is much less frequent than in the brain, but may occur 
either as capillary apoplexy or as larger apoplectic clots. Capil- 
lary haemorrhages, similar in appearance to those of the brain, may 
occur as the result of injury, or near areas of softening or tumors, or 
may accompany severe convulsions, as in tetanus. Apoplectic clots, 
which are comparatively rare in the spinal cord, are usually small, 
commonly not more than one cm. in diameter, and are similar in 
their appearances, and in the changes subsequent to their forma- 
tion, to those of the brain. They are usually the result of injury ; 
but they may occur spontaneously, probably in most cases as a result 
of inflammation, and are then most apt to occur in the gray matter. 
Sometimes, however, hemorrhagic foci are found in the spinal cord 
without traumatism or evidence of inflammatory change. 

HtEMATOMYELIA and h^ematomyelopore. 

Several cases have been described in which long tubular canals 



392 



THE SPINAL CORD. 



were found in the spinal cord. These have been considered the 
result of central necrosis, myelitis, etc., varieties of syringomyelia, 
and variously named. These long cavities have no well-defined 







r ■: a 






Fig. 182.— Section op the Spinal Cord showing Hemorrhage into the Gray Matter and 
Extending Lengthwise of the Cord. 

Showing an early phase of hsematomyelopore. (Van Gieson.) 



I 



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$ ; $&&%w 



Fig. 183.— H^EMATOMyELOPORE. (Van Gieson.) 
The section shows at one point a cyst-like cavity in the spinal cord, originating in a haemor- 
rhage in the posterior root and extending nearly the entire length of the cord. The sides of the 
cavity are now covered with tissue detritus. 

wall and no distinct lining membrane. They are filled with blood 
and tissue detritus. 

Van Gieson has shown that they correspond to columnar hsemor- 



THE SPINAL CORD. 393 

phages within the cord, usually following traumatisms in which the 
blood forced its way lengthwise of the cord, forming columnar masses. 
On the absorption of this blood the long cavities or canals are left. 
This condition Van Gieson has called hcematomyelojjore. 

INJURIES. 

The spinal cord, may be compressed or lacerated by penetrating 
wounds, by fracture or dislocation of the vertebrae, or by concussion 
without injury to the vertebrae. The spinal cord is found simply 
disintegrated, or there may be much haemorrhage and the disinte- 
grated nerve tissue be mixed with blood. If life continue, the nerve 
elements may degenerate; Gluge's corpuscles and free fat droplets 
may form; blood pigments may be formed; and when inflammation 
supervenes more or less pus may be intermingled with the degen- 
erated detritus. There may be marked changes in the minute 
structure of the cord, without any change being evident to the 
naked eye. 

SECONDARY DEGENERATIONS IN THE SPINAL CORD. 

The modern conception of the structural elements of the nervous 
S}'stem is that they are complex cell units called neurons, which may 
extend over long distances, and although without direct anastomoses 
stand in intimate topographical and functional relationships with one 
another. 

The neuron consists of a cell body, an axis-cylinder process, the 
neuron, and protoplasmic processes of the cell called dendrites. 

A destruction of the cell body or a separation of the processes from 
the cell body is accompanied by a degeneration of the processes. 

The cell bodies are grouped together in the gray matter of the 
brain and cord and in the ganglia situated along the peripheral nerves. 

Through the dendrons impulses are conducted to the cell bodies; 
through the axis-cylinder processes they are conducted from the cell 
body. 

When the cell bodies of the neurons of certain parts of the brain 
and of the spinal cord are destroyed, or when the motor nerves lead- 
ing from them are severed or seriously injured, that portion which is 
deprived of or separated from its cell body degenerates. 

After a time — frequently two to four weeks — the medullary sheath 
and axis cylinder disintegrate, becoming granular and fatty. These 
products of degeneration may be in part absorbed at once, or may 
collect in cells, forming the so-called compound granular corpuscles. 
After a still longer time — sometimes several months — the degenerated 
32 



394 THE SPINAL CORD. 

areas become gray in color from the absorption of the degenerate 
myelin, harder, and somewhat shrunken. These changes are parti 
due to the formation of new connective tissue which takes the plac 
of the degenerated nerve fibres. 

Since the affected portion of nerve tissues becomes gray or tram 
lucent after the myelin is broken down and absorbed, and the ne" 
connective tissue is formed, this is often called Gray Degeneration 
or, as the degenerated areas are harder than normal, it is sometim( 
called Sclerosis. 

Now, it is found that this secondary degeneration takes pla( 
in the direction in which the fibres conduct — in centripetal or sei 
sory fibres, upward ; in centrifugal or motor fibres, downwarc 
Thus we have Descending Secondary Degeneration (Descendin 
Sclerosis), and Ascending Secondary Degeneration (Ascendin 
Sclerosis). 

Descending Secondary Degeneration. — This change affec 
chiefly the motor nerve fibres, and may reach but a short distanc 
from the seat of lesion, or may extend for a long distance, dependin 
upon whether the severed fibres run a short or long course befoi 
reaching their termination. Lesions of the brain, such as emboli 
softenings and apoplectic clots, which destroy or interrupt any of tt 
motor nerve fibres originating in the Central convolutions, may I 
followed by degeneration of the portion of the fibres situated peripl 
erally to the lesion. These fibres pass through the corona radiate 
anterior portion of the internal capsule, pes pedunculi, pons, an 
thence to the anterior pyramids, where most of them decussate an 
pass to the posterior part of the lateral columns of the opposite sid< 
Those which do not decussate form a narrow band at the inner pa] 
of the anterior columns of the same side, constituting the column 
of Tilrck. These fibres which convey motor impulses from the brai 
to the cord form a system called the pyramidal tract. 

Now, a lesion in the brain separating the motor nerve fibres of or 
side from their cells of origin in the motor cortex will be followed b 
areas of degeneration in the posterior part of the lateral column c 
the opposite side, and in a narrow band near the anterior longiti 
dinal fissure of the same side (see Fig. 184). A lesion below tb 
medulla, involving the fibres of the pyramidal tract on one side, wi 
be followed by degeneration of the fibres on the same side below th 
point of lesion. If a part only of the fibres in any of these regior 
is interrupted the amount of degeneration is of course proportior 
ately small. 

Ascending Secondary Degeneration. — Any lesion interrupting 
the course of the centripetal (mostl}' sensory) nerve fibres in the cor 
is followed by degeneration of the central ends of the involved fibres 



THE SPINAL CORD. 395 

because these are separated from their cells of origin either in the 
spinal ganglia or in the gray matter of the cord itself. 

Part of these sensory fibres — some of which are short, others long — 






Fig. 184.— Descending Secondary Degeneration. 
Section of cord in cervical region. Degeneration of the column of Tiirck and of the crossed 
pyramidal tract. 

are situated in the posterior columns and form communications be- 
tween different parts of the gray matter. 



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Fig. 185.— Ascending Secondary Degeneration in the Spinal Cord (Upper Cervical Region). 
After fracture of the spine destroying the eighth cervical segment; the lesion involves the 
columns of Goll, the direct cerebellar tract, and the columns of Gowers. 

Others of the sensory fibres are grouped in a narrow band near 
the posterior longitudinal fissure, forming the columns of Goll, 



396 THE SPINAL CORD. 

while other sets, forming the so-called direct cerebellar tract anc 
the columns of Gowers, are situated in the periphery of the latera 
columns. 

A lesion of the cord involving the severance or destruction ol 
these centripetal fibres will be followed by ascending degeneration oi 
the direct cerebellar tract and of the columns of Goll and Gowers and 
of the entire posterior column, just above the lesion (Fig. 185) . The 
degeneration may be traced along the columns of Goll to the resti- 
form bodies, and in the cerebellar tract to the cerebellum. Lesions 
involving the entire thickness of the cord will produce bilateral 
degenerations. 

Following the secondary degeneration of the nerve fibres, whethei 
ascending or descending, new connective tissue may form, filling the 
space formerly occupied by the nerve elements (Fig. 186). 

This new connective-tissue development was formerly looked uporj 
as the primary factor in various forms of sclerosis in the central 
nervous system to which the nerve changes were secondary ; but the 




Fig. 186.— Ascending Gray Degeneration. 
A small portion from edge of degenerated region of cord shown in Fig. 185, more highlj 
magnified. A, normal nerve fibres ; B, degenerated area. 

new knowledge on the subject makes it evident that the connective 
tissue should be looked upon not as a chronic interstitial inflamma- 
tion, but as the result of a replacement fibrous hyperplasia. 

PROGRESSIVE SPINAL MUSCLE ATROPHY. 

Degeneration or atrophy of the anterior nerve cells of the spinal 
cord and their neuraxons may be associated with varying degrees of 
atrophy of the corresponding muscles — progressive spinal muscle 
atrophy. 

BULBAR PARALYSIS. 

Similar changes in the cells of the motor nuclei of the medulla 
may be associated with paralysis of the tongue, lips, and larynx, and 
constitute the so-called bulbar paralysis. 

AMYOTROPHIC LATERAL SCLEROSIS. 

Under obscure conditions there may be degenerative changes of 



THE SPINAL CORD. 397 

both the central motor neurons from the brain to the cord and of the 
peripheral motor neurons from the motor cells of the cord to the 
.muscles. These conditions determine a replacement fibrous hyper- 
plasia (sclerosis) in the lateral column and also in the anterior cornua 
of the spinal cord. If small groups of neurons are involved the 
sclerosis may be slight. This condition has been called amyotrophic 
lateral sclerosis (Fig. 187). 

It should be borne in mind, in looking for these secondary lesions, 
ihat they are not developed until considerable time has elapsed since 
the development of the primary lesion, and that when small areas 






Fig. 187.— Section of Spinal Cord in Amyotrophic Lateral Sclerosis. 
Shows degeneration of the crossed pyramidal tracts on both sides. 

;are involved they are usually inconspicuous. In any event, the 
lesions are apt to be more evident to the naked eye in specimens 
Iiardened in chromic fluids than when fresh, and microscopical 
examination is often necessary for their recognition. . 

INFLAMMATION. 

Acute Myelitis. 

This lesion of the spinal cord, which is sometimes distinctly in- 
flammatory in character and sometimes of a degenerative nature, 
is usually confined to a comparatively limited longitudinal extent 
of the cord, and hence is sometimes called transverse myelitis. 
When the cord is removed and laid upon the table, if the lesion 
is marked, a flattening of the cord at its seat may be observed ; or 
•on passing the finger gently along the organ the affected segment 
will be found softer than the rest of the cord. On making a section 
through the diseased portion the nerve tissue may be white or red 



398 THE SPINAL CORD. 

or yellowish or grayish ; it may be quite firm, but is usually more 
or less softened and sometimes almost diffluent. 1 

Microscopical examination shows different appearances, depend- 
ing upon the stage of the inflammatory or degenerative process. 
There may be much blood, or, if the lesion has existed for some time, 
blood pigments ; also fragments of more or less degenerated nerve 
fibres and ganglion cells (Fig. 188), myelin droplets, free fat granules, 
and larger and smaller cells filled with fat granules (Gluge's corpus- 
cles) , pus cells, granular matter, neuroglia cells, and sometimes cor- 
pora amylacea. The various combinations of these elements give 
rise to the different' gross appearances which the diseased part pre- 
sents. In earlier stages of the lesion the blood vessels may be 
dilated, the nerve fibres and cells swollen; or the walls of the blood 
vessels may be thickened or fatty, or surrounded by a sheath of leu- 




Fig. 188.— Degenerated Tissue from Acute Myelitis. 

oocytes and cells derived from the connective-tissue cells of the ad- 
ventitia. 

The lesion is apt to commence in the gray matter or at its edge, 
and then extend first laterally and afterward upward and downward. 

In a certain number of cases the degenerated material may be 
absorbed and a cicatrix or cyst formed. In the least extensive forms 
of the lesion there is apparently a regeneration of the nerve fibre, 
and a restoration of the functions of the cord. 

Secondary gray degeneration, both ascending and descending, 
may occur in the form of myelitis, varying in extent according to the 
size of the primary lesion. 

Acute disseminated myelitis runs a rapid course, and proves 
fatal in a short time. The inflammation may involve nearly the 
whole length of the cord, but is more intense in some places than in 
others. The cord is swollen and congested, it is infiltrated with pus 

1 It should be remembered that a mechanical injury to the cord in removal, such 
as crushing or bruising, may reduce the injured portion to a pulpy consistence and 
thus produce appearances somewhat similar to those of some forms of inflammatory 
softening (see p. 381). 



THE SPINAL CORD. 



399 



cells, the connective-tissue framework is swollen, and the nerve ele- 
ments are degenerated (see Poliomyelitis). 

Poliomyelitis Anterior {Myelitis of the anterior horns). — This 




Fig. 189.— Poliomyelitis Anterior. 

Showing degenerated area in anterior cornua, with atrophy of gray matter. A, Atrophic 
region. Specimen prepared by Dr. Ira Van Gieson. 

name is applied to a group of cases which are characterized by clini- 
cal symptoms indicating changes in the anterior gray cornua. The 
disease occurs both in children and in adults, and varies in the 










Fig. 190.— Poliomyelitis anterior. 
Showing portion of Fig. 189 at edge of affected area, more highly magnified. A. normal 
ganglion cells surrounded by nerve fibres ; B degenerated ganglion cells ; C, granular masses at 
place of ganglion cells ; D, small cavity containing fluid 



400 THE SPINAL CORD. 

severity, acuteness, and duration of its symptoms. In many cases 
there is complete recovery , and then we must suppose that the changes 
in the nervous tissue were not destructive in their character. In 
other cases the symptoms are more permanent, indicating a destruc- 
tive lesion. From the autopsies so far recorded we learn that the 
lesion is most frequent at the lumbar and cervical enlargements of 
the cord, but may occur anywhere, and is often in scattered patches 
(Fig. 189). There is degeneration, shrinkage, pigmentation, and 
atrophy of the ganglion cells in the anterior gray cornua (Fig. 190). 
The chromophyllic masses in the ganglion cell bodies may be disin- 
tegrated and in various ways altered (see page 376). There may be 
an increase of connective tissue in the gray cornua and in the anterior 
and lateral columns. There may be degeneration and destruction of 
a considerable part of the anterior cornua; there may be atrophy of 
the anterior nerve roots. The cord may be considerably distorted as 
the result of the lesion. 

There is evidence that the lesion in many of the cases of so-called 
Landry's paralysis are those of acute myelitis or of poliomyelitis, 
involving important changes in the ganglion cells. 1 



CHRONIC MYELITIS. 

Chronic Interstitial Myelitis. — Under this heading are em- 
braced a variety of lesions which probably differ from one another 
somewhat in the nature of the changes involved, but more in the seat 
of the disease. We shall consider without special classification the 
most important forms. 

Chronic Transverse Myelitis. — In certain cases of pressure on 
the spinal cord from a tumor or from displacement of the bones of 
the vertebral column, etc., instead of becoming softened or under- 
going acute inflammatory changes, the cord becomes the seat of a 
localized formation of new connective tissue, with consecutive atro- 
phy of more or less of the nerve elements in the gray and white 
matter. The cord becomes in this way harder, and sometimes 
shrunken at the seat of lesion, and grayish in color. This change 
may be followed by ascending and descending gray degeneration. 

Multiple Sclerosis. — This lesion, similar in its nature to multi- 
ple sclerosis of the brain, often occurs with it. It consists in the 
formation, in more or less numerous scattered, circumscribed areas, 
of new connective tissue, apparently derived from the neuroglia. 
The formation of new connective tissue is preceded or accompanied 
by degeneration and atrophy of the nerve fibres and ganglion- cells. 
The new connective tissue consists of the characteristic branching 

1 Consult Bailey and Eicing, New York Medical Journal, July, 1896. 



THE SPINAL CORD. 401 

neuroglia cells, surrounded by a more or less dense network of fine 
fibrillae, many if not most of which seem to be branches of the neu- 
roglia cells. Corpora amylacea and sometimes fat droplets, either 
free or contained in cells, may be present in the sclerosed areas. 



;te. 









■M 



/ 




Fig. 191.— Multiple Sclerosis in Spinal Cord. 
Showing larger and smaller areas of atrophy of nerve elements with formation of connective 
tissue. 

The areas of sclerosis may involve both gray and white matter, 
and may be very small or large (Fig. 191). If very small or in early 
stages of formation, they may not be recognizable by the naked eye, 






*&•■ 



Fig. 192.— Posterior Spinal Sclerosis (Tabes Dorsalis). 
Section of the spinal cord in the cervical region. 

but when visible they are grayish, translucent, and firmer than the 
surrounding tissue, and may or may not present a depressed sur- 
face; they sometimes project above the general level. The cause of 



402 



THE SPINAL CORD. 



this, as of other forms of so-called idiopathic interstitial myelitis, is 
very obscure. 

Posterior Spinal Sclerosis (Locomotor Ataxia; Tabes Dor- 
salis). — The lesions of this condition consist essentialry of degener- 
ation in the peripheral sensory neurons, especially in the spinal gan- 
glia and posterior roots. This change involves degeneration and 
atrophy in greater or less degree of the nerve fibres in the posterior 
columns of the spinal cord and an associated replacement fibrous 
hyperplasia or sclerosis (Fig. 192). 

Not infrequently the posterior portion of the lateral columns are 
also involved. Exceptionally a large part of the lateral columns is 
involved, and also the anterior cornua. The change usually com- 




THS 



Fig. 193.— Posterior Spinal Sclerosis. 
A portion of sclerosed area in the posterior columns of the spinal cord, 
nective tissue; 6, blood vessels; c, nerve fibres; d, atrophied nerve fibres. 



a, New formed con- 



mences in that portion of the posterior columns bordering on the 
posterior cornua, but may involve, as above stated, the adjacent 
parts. It is usually most marked in the lower dorsal and lumbar 
regions. The sclerosis may extend upward to the restiform bodies, 
but in the cervical region it is apt to be confined lagely to the columns 
of Goll, although there are exceptions to this. 

When the lesion is well developed the pia mater over the affected 
area is usually thickened and adherent to the cord. In its early 
stages there may be no change evident to the naked eye ; but when 
advanced the posterior columns may appear somewhat depressed, and 
grayish and firmer than the rest of the cord. The microscopical ap- 
pearances vary, depending upon the stage and extent of the lesion. 



THE SPINAL CORD. 403 

The walls of the blood vessels may be thickened; there is more or less 
new connective tissue consisting of neuroglia cells and very numer- 
ous interlacing, delicate fibrils. There may be numerous corpora 
amylacea and fat granules, either free or collected in cells. The 
nerve fibres may be numerous, but separated more or less widely by 
the new connective tissue, or they may be very few in number and 
irregularly scattered through the new tissue (Fig. 193) . The atrophy 
may involve the fibres of the posterior nerve roots and cornua, and 
even the ganglion cells of the latter. The peripheral nerves and the 
cells of the spinal ganglia may be degenerated. 

According to the researches of Lisauer, 1 the columns of Clarke 
in the dorsal region show in this disease a -very constant and marked 
diminution in the number of delicate fibrils which under normal 
conditions surround the ganglion cells. 

In the rare cases in which the sclerosis extends to the lateral 
columns and to the anterior cornua, the minute characters of the 
lesions are the same. There is much reason for the belief that the 
formation of connective tissue in tabes is not the primary factor in 
the disease but is secondary to degeneration of the nerve fibres in the 
involved portion cf the cord, and is thus in the nature of a replace- 
ment connective-tissue hyperplasia or fibrosis. 

Solitary tubercles and gummata may occur in the spinal cord,, 
but are not common. 

TUMORS. 

Cysts may occur as a result of softening or from unknown causes. 
Sometimes very long, narrow canals are found in the spinal cord, 
even reaching nearly its whole length. Some of these are evidently 
the dilated central canal, as they are lined with epithelium. Others, 
however, doubtless originate in haemorrhages (see Haematomyelo- 
pore, p. 391). 

In the pia mater of the cord are sometimes found small fibromata^ 
osteomata, and lipomata. 

Endotheliomata, of the same types as have been described as 
existing in the pia mater of the brain, are much more rarely found 
in the pia mater of the cord . 

A fatty sarcoma 2 of the pia mater, which infiltrated the cord, 
formed a tumor as large as a filbert, and had for twelve years caused 
gradually increasing paraplegia, has been described. 

Two curious cases 3 of diffuse sarcoma and one of endothelioma of 
the pia mater of the whole length of the cord are recorded. The}' 

1 Fortsghritte der Medicin, Bd. ii., 2s o. 4, 1884. 

J Trans: Lond. Path. Soc, xxxix. 

a Trans. London Path. Soc, xxxviii. ; Arch, fur Psych., 1885. 



404 



THE SPINAL, CORD. 



occurred in girls of 4|, 16, and 22 years of age. In each case the pia 
mater of the whole length of the cord was diffusely thickened and 
studded with nodules. In two of the cases the growth was composed 
of round cells, in the third case of large endothelial cells arranged in 
alveoli. In two of the cases the clinical symptoms lasted only for 
about three weeks, in the third case for five months. The acuteness 
of the symptoms was such as to indicate the existence of spinal men- 
ingitis. 

In the spinal cord itself gliomata, fibromata, sarcomata, glio-sar- 
comata, and angio-sarcomata occur, but are rare. 

When gliomata or glio-sarcomata do occur in the spinal cord, the 
new growth is apt to extend for some distance lengthwise in the cord 
and to be attended with the formation of a cavity ; this condition is 
usually described under the name of syringomyelia. 




Fig. 194.— Syringomyelia. 
Transverse section of cord. A, white substance of cord, distended by tumor; B, B, dis- 
torted and atrophied gray substance of anterior cornua; C, tumor mass (glio-sarcoma) ; D, 
cavity in cord. Drawn from specimen prepared by Dr. Van Gieson. 



SYRINGOMYELIA . 

This lesion of the spinal cord consists in the formation of glio- 
matous or glio-sarcomatous tissue in the vicinity of the central canal, 
and its subsequent partial disintegration with the formation of one or 
more cavities within the substance of the cord (Fig. 194). These 
cavities, which are filled with fluid, vary greatly in size, shape, and 
extent, and, while usually situated in the central region of the cord, 
they may involve the anterior and posterior cornua and invade the 
posterior columns. There may be two communicating cavities, and 
these may, but usually do not, open into the central canal. The lon- 
gitudinal extent of these cavities varies greatly. The lower cervica] 
and upper dorsal regions are most frequently involved. The cavity 
is usually lined with tissue somewhat denser than that which makes 



THE SPINAL CORD. 405 

up the bulk of the tumor. The gliomatous or glio-sarcomatous tissue 
which forms the basis of the lesion in syringomyelia probably origi- 
nates from the layer of neuroglia which surrounds or extends away 
from the central canal. 

Syringomyelia is frequently mistaken for hydromyelia (see below), 
which is a congenital malformation, and in which the longitudinal 
cavity in the cord is at some period lined with epithelial cells. 
Syringomyelia has also been confused with hsematomyeloporp (see 
page 392)." 

There seems, furthermore, to be a class of lesions of the cord, 
usually classed as syringomyelia, in which cavities of various forms 
co-exist with a tumor in the vicinity of the central canal. But these 
cavities do not appear to be formed by a breaking down of the tumor 
tissue, but in some other way as yet little understood. 

MALFORMATIONS. 

The malformations of the spinal cord may be conveniently classed 
as follows (Van Gieson) : ' 

I. Congenital Deformities Associated with Monstrosi- 
ties, and Incompatible with Extra- Uterine Life. 

These may be divided into : 

1. Amyelia, or absence of the spinal cord. This is almost in- 
variably associated with absence of the brain. 

2. Atelomyelia, or partial development of the spinal cord. This 
is often seen in the anencephalous or acephalic monsters, where, cor- 
responding to the incompletely developed brain, there may be various 
degrees of defective development in the length of the cord. 

3. Diastematomyelia, a condition in which a portion of the 
whole of the cord is split into two lateral halves. Each half of the 
cord, being enveloped in its own membranes and giving rise to its 
own nerve roots, may fuse together to form a single cord at some 
region. 

4. Diplomyelia, or a formation of two spinal cords — a duplication 
of the spinal cord. This happens in the various kinds of double 
monsters. 

II. Minor Congenital Malformations not Inconsistent 
with the Maintenance of Life. 

1. Hydrorrhachis interna is a defective closure or arrangement 
of the divisions of the primary foetal central canal often resulting in 
the dilatation of the central canal by fluid {Hydromyelia) Fig. 195). 
This dilatation may be moderate, or so extreme that but little of the 
substance of the cord is left as a thin shell around the central cavity. 

1 Van Gieson, "Artefacts of the Nervous System, " New York Medical Journal, 
1892. 



406 



THE SPINAL CORD. 



When they have not been destroyed by atrophy, epithelial cells may 
be found lining the cavity. 

This condition may be accidentally found after death. Its pres- 
ence may also be indicated by its association with spina bifida. 1 




Fig. 195.— Hydromyelia. 
In the section from which this drawing was made, the epithelial cells surrounding the di- 
lated central canal were well preserved. 

2. Heterotopia, or misplacement of the substances of the cord, 
(a) There may be misplaced portions of the gray matter. 

(6) Portions of the white matter may be arranged in an unusual 
manner. 

3. Anomalies of the Spinal Nerve Roots. 




Fig. 196.— False Heterotopia. Section from Cervical Region op Spinal Cord. 
Showing artificial displacement of the structures by an experimental bruise ("false hetero- 
topia "J after the removal of the cord from the body. (Van Gieson.) 



1 Under this subdivision the condition known as hydrorrhachis externa may be 
conveniently alluded to, which consists in an abnormal congenital accumulation of 
fluids between the meninges of the cord, causing more or less diminution in the 
volume of the latter. 



THE SPINAL CORD. 407 

4. Asymmetries of the Spinal Cord. 

III. Malformations of the Spinal Cord Acquired during 
Extra-Uterine Life or Secondary to Defective Develop- 
ment in other Parts of the Body. 

1. Distortions following other cord lesions. 

2. Asymmetry of the cord due to arrested development after birth 
or to secondary atrophy of portions of the cord in association with 
defective development or absence of some other part of the body. 

3. Asymmetry of the cord with congenital defects of the extremities 
or muscles, such as intra-uterine'or other amputations, clubfoot, etc. 

4. Variations in the volume of the cord as a whole. 

False Heterotopia. — Congenital displacement of the gray or white 
matter of the spinal cord — heterotopia — has been frequently de- 
scribed. Van Gieson ] has shown, however, that in a large propor- 
tion of cases the so-called heterotopia is an artefact (Fig. 196) and 
has been caused by bruises or careless handling of the cord during 
its removal from the bod}' or in the process cf examination or hard- 
ening. 

Spina bifida. — In the majority of cases hydrorrhachis is ac- 
companied by a more or less complete lack of closure of the spinal 
canal posteriorly, so that the collections of fluid within may pouch 
outward through the opening in the form of a sac. The sac may 
be covered by skin, or this may be absent, either from the begin- 
ning or as a result of thinning and rupture. The walls of the 
sac may consist of the dura mater and the pia mater, or, in cases 
of hydrorrhachis externa, of the dura mater alone; when both 
are present they are usually more or less fused together. Inside of 
the membranes of the sac there may be a shell of distended nerve 
tissue of the cord ; or the spinal cord may be split posteriorly and the 
sides crowded sideways ; or there may be a rudimentary fragment of 
the cord suspended in the sac or attached to the walls ; or the cord 
may be but little changed and remain inside the spinal canal. The 
openings in the spinal canal may be due to the complete or partial 
absence of the vertebral arches, or more rarely the sac may protrude 
through openings between the completely formed arches. Spina 
bifida most frequently occurs in the lumbar and sacral regions, but 
it may occur in the dorsal or cervical regions, or the canal may be 
open over its entire length. Very rarely it is open on the anterior 
surface. The protruding sac may be very small or as large as a 
child's head. The fluid in the sac is usually clear, but may be turbid 
from flocculi of degenerated nerve tissue. 

1 Tan Gieson, loc. cit. 



408 THE SPINAL CORD. 

THE PERIPHERAL NERVES. 

CHANGES IN NERVES AFTER DIVISION. 

When nerves are divided or a portion destroyed by injury, the 
nutrition of certain parts of the fibres is interfered with, apparently 
because of the separation of these from their neurons, and they suffer 
degeneration ; but after a time, if the conditions be favorable, they 
may undergo regeneration and restitution of function. The degene- 
ration not only affects the entire severed portion, but it occurs at. 
nearly the same time in all parts. The degeneration consists in 
the breaking-up of the medullary sheaths into variously shaped 
droplets, and the decomposition of these, with the formation of fat, 
which may remain for some time either free or enclosed in cells, and 
finally be absorbed (see Fig. 197). The axis cylinder, too, is, in many 
cases at least, more or less completely destroyed. The neurilemma 
and its nuclei do not seem usually to undergo degeneration, but may 
persist and take part in the regeneration of the nerve when restitu- 
tion occurs. 

After a variable time, if the conditions are favorable, the divided 




Fig. 197.— Degeneration of Nerve Fibres in Multiple Neuritis. 
From a case of alcohol poisoning. Specimen stained with osmic acid. The broken-down 
medullary sheath and fat droplets are stained deep black. 

ends of the nerve may be united, and a regeneration or new forma- 
tion of nerves in or about the severed portions may occur, so that the 
function may be resumed. Considerable time is required, frequently 
months, for the completion of the regenerative process. Degenera- 
tion of the nerves not only follows mechanical injuries, such as inci- 
sion, crushing or tearing, and compression, as from a tumor or dis- 
location of the bones, but it may result from disease of the special 
nerve centres with which the nerves communicate, or from inflam- 
mation of the nerves themselves. 

INFLAMMATION. 

Acute Exudative Neuritis. — Primary acute inflammation of 
the nerves may occur as the result of injury, or it may be secondary 
to an inflammatory process in its vicinity, although, owing to the 
dense lamellar sheaths and the special blood supply, the nerve trunks 
may escape participation in even very severe inflammatory processes 



THE SPINAL CORD. 403 

in surrounding tissues. The inflamed nerve may be red and swollen 
and infiltrated with serum and pus cells. The process may undergo 
resolution or terminate in gangrene and destruction of the nerve, or 
it may become chronic and result in the formation of new connective 
tissue. 

Degeneration and regeneration of the nerve fibres, similar to 
those above described as following division of nerve trunks, may oc- 
cur in acute neuritis. 

Chronic Interstitial Neuritis.— -This is essentially a chronic in- 
terstitial inflammation resulting in an increase of connective tissue in 
the nerve sheath and intraf ascicular bands. As a result of this the 
nerve fibres undergo atrophy from pressure ; the medullary sheath, 
and finally the axis cylinder, being, in more or less of the fibres, par- 
tially or completely destroyed. 

Multiple Neuritis. — Under a variety of conditions, such as ex- 
posure to cold and wet, overexertion, poisoning by alcohol, arsenic, 
lead, etc., and in connection with the acute infectious diseases, a de- 
generation of the nerve fibres in various parts of the body may occur 
(Fig. 197), which may be accompanied with or followed by prolifera- 
tive changes in the neurilemma cells. Regeneration of the affected 
nerve fibres may occur under these conditions, as after experimental 
division of the nerves, leading to their restitution. 1 In some forms 
of multiple neuritis the inflammation is exudativa in character, and 
new cells of various forms are found within and between the nerve 
fibres. The exact part which the neurilemma and other intrafasci- 
cular cells play in the inflammatory and regenerative changes of 
nerves is not yet very fully made out. 

Syphilitic and Tuberculous Inflammation of the nerves is not 
common except at their central ends, in connection with similar in- 
flammations of the meninges, or when they are secondarily involved 
in connection with these inflammations in neighboring tissues. 

Leprous Inflammation. — This consists in the formation within 
the nerve of masses of new-formed tissue somewhat resembling 
granulation tissue, in whose cells multitudes of characteristic bacilli 
are uniformly found (see Leprosy). It constitutes the variety of 
leprosy known as lepra anaisthetica. 

TUMORS. 

The tumors of the nerves are such as consist largely of or con- 
tain new-formed nerve tissue — true neuromata ; and the so-called 

Consult Starr, "Multiple Neuritis." The Middleton Goldsmith Lecture for 
1887. Trans. New 'York Pathological Society, 1887, p. 1. 
33 



410 THE SPINAL CORD. 

false neuromata (Figs. 141 and 142), which are for the most part 
fibromata or myxomata of the connective tissue of the nerve. 
Myxo-sarcomata are less common, and primary sarcomata rare. 
The nerves may be secondarily involved in sarcomata or carcino- 
mata, though not infrequently nerves pass through these tumors 
without being in the least involved in their peculiar structure. Pal- 
tauf has described as endotheliomata rare tumors of the glandula 
carotica. 1 

ACROMEGALIA. 

This rare disease is especially characterized by an overgrowth 
of the termiDal portions of the extremities and of the bones of the 
face. But there may be a general involvement of the skeleton. This 
excessive growth is in the diameter and not in the length of the bones, 
accompanied by local exostoses, and is associated with an overgrowth 
of the soft parts composing the involved extremities. A marked 
enlargement of the pituitary body has been found in some of the 
cases, and this has been claimed to be the causative factor in the 
nutritional abnormality leading to the hypertrophic lesions of the 
bone. 2 

SCLERODERMA. 

Under little understood conditions a sharply circumscribed or 
widely extended hardening of the skin may occur as the result of a 
swelling of the old and formation of new connective tissue in the 
skin. This is associated with thickening of the walls of the blood 
vessels. The new-formed tissue may contract, it may continue to 
form so that the lesion is progressive; or, cessation of the process and 
recovery may occur. 3 



METHODS OF PREPARATION OF NERVE TISSUE FOR MICROSCOPICAL 

STUDY. 

The general methods of hardening have already been given on pages 
18 and 21. For minute study there is no one method of staining and 
mounting upon which we can rely exclusively for the study of all 
lesions. A preliminary examination of areas of inflammatory soft- 
ening, or of the disintegrated tissue in apoplectic clots, or of the 
new-formed tissue in chronic hoemorrhagic pachymeningitis inter - 

1 Paltauf, Ziegler's Beitrage zur path. Anatomie, etc., Bd. xi., p. 260, 1882. 

2 For a careful description of a case and a discussion of its relationships to similar 
abnormalities consult Arnold, "Acromegalic, Pachyacrie oder, Ostitis, " Ziegler's 
Beitr. z. path. Anat., Bd. x., 1891. 

3 Lewin and Heller, "Die Sclerodermic, " Berlin, 1895, bibliography. 



THE SPINAL CORD. 411 

na, may be made by teasing portions of the affected tissues in one-half - 
per-cent salt solution. Or the tissues in these lesions, or in any others 
in which fatty degeneration is suspected, may be placed for twenty- 
four hours in one-per-cent aqueous solution of osmic acid, and then 
washed and teased in glycerin. In this way the myelin and the fat 
will be stained brown or black. Secondary and other degenerations 
of medullated nerves may be studied by soaking the nerves for 
twenty-four hours in one-per-cent solution of osmic acid, and then 
staining with picro-carmin and teasing and mounting in glycerin. 
Suppurative inflammation of the central nervous system and its 
membranes, or the connective-tissue changes in general, may be 
studied in sections from the tissues hardened in M tiller's fluid and 
alcohol, stained double with hsematoxylin and eosin (see page 60), 
and mounted in Canada balsam. 

A very useful method of staining sections of nerve tissue, espe- 
cially of the brain and cord, is that known as Weigert's hsematoxy- 
lin method. The tissue is first well hardened in Mtiller's fluid. 

Blocks of the hardened tissue are embedded in celloidin and sec- 
tions made in the usual way. The sections are first soaked for 
twenty-four hours in a saturated aqueous solution of neutral cupric 
acetate diluted with an equal bulk of water. They are now thoroughly 
washed twice in water, then in alcohol, and then are tiansf erred to 
the hsematoxylin solution, made as follows : 

Hsematoxylin crystals 1 gm. 

Alcohol, 97 per cent 10 c.c. 

"Water . a \ 90 " 

Saturated aqueous solution Lithium Car- 
bonate 1 " 

In this solution the sections remain for two hours. (If the finer 
fibres of the cerebral cortex are to be brought out the sections must 
remain for twenty-four hours in the hsematoxylin solution.) The 
sections are now thoroughly washed in two or three waters and 
transferred to the bleaching solution, composed as follows : 

Potassium Ferricyanid 2.5 gm. 

Sodium Biborate 2. " 

Water 200 c.c. 

In this flnid the sections discharge a brownish color, and they 
remain in it until the gray matter has a distinct yellow color and 
the white matter is bluish-black. The time required to produce this 
effect varies considerably, and is usually from half an hour to an 
hour. The sections are now washed, dehydrated with alcohol, 



412 THE SPINAL CORD. 

cleared up in oil of cloves or oil of origanum, and mounted in bal 
sam. The sections may be stained in alum carmine before dehy 
dration, to bring out the nuclei. In sections stained by this metho* 
the gray matter, connective-tissue elements, and ganglion cells hav 
a yellow or yellowish-brown color, the axis cylinders are uncolored o 
have a slight yellowish tint, while the medullary sheaths are bluist 
black or black. 

To demonstrate the presence of miliary aneurisms in or abou 
apoplectic clots, it is usually necessary to macerate the brain tissue i: 
water until the nerve elements disintegrate, and they may then b 
washed away under a stream of water, leaving the blood vessels wit 
their aneurisms exposed. 

Nissl's Staining Method. — There are several variations of thi 
method, but the following gives good results in most cases: 

The essential feature of the so-called Nissl's method is the appl: 
cation of the anilin dyes to the staining of certain structural elemenl 
in the nucleus and cytoplasm, which are distinguished from the othe 
structures of the cell by a differentiating decolorization with alcohol 

Methylen blue is the most generally useful of the anilin dyes fc 
this purpose. 

The specimens should have been carefully hardened in sublimat 
solution or in alcohol or in formalin. 

Very thin sections are stained in one-per-cent solution of methj 
len blue. The staining may be effected on a slide on which the sec 
tions are floating in the blue solution by gently heating over a lam 
until the fluid steams. 

The sections are now transferred to a mixture of absolute alcohc 
90 parts, with anilin oil 10 parts, in which the differentiation i 
effected by the use of successive fresh portions of fluid until slight bu 
distinct differentiation in color is seen between the gray and whit 
matter of the nerve tissue. The exact degree of decolorization whic 
gives the best pictures will be learned by practice of the method 
The sections are now freed from the bulk of the alcohol upon th 
slide, cleared in xylol, and mounted in dammar varnish, in which th 
color is apt to be preserved better than in balsam. By this procednr 
the chromosomes and the chromphylic bodies in the cytoplasm c 
ganglion cells are sharply differentiated, and thus abnormal condi 
tions may be detected in them (see Fig. 178). 

The applications of this method of staining to other cells tha] 
those of the nervous system are wide and of great promise. 



THE KESPIBATORY SYSTEM. 



THE LARYNX AND TRACHEA. 
MALFORMATIONS. 

The larynx and trachea may be entirely absent in acephalic mon • 
sters. The larynx may be abnormally large or small. The epiglot- 
tis also may be too large or too small, or may be cleft. There may 
be communications between the trachea and the oesophagus, and then 
the pharynx generally ends in a cul-de-sac, and the oesophagus opens 
into the trachea. There may be imperfect closure of the original 
branchial arches, so that there are fissures in the skin leading into 
fistulse which open into the pharynx or trachea. The fissure in the 
skin is small and is situated about an inch above the sterno-clavicu- 
lar articulation, usually on one or both sides, more rarely in the mid- 
dle line. Individual cartilages, as the epiglottis, or one or more 
rings of the trachea, may be absent, or there may be supernumerary 
rings. The trachea may divide into three main bronchi instead of 
two, and in that case two bronchi are given off to the right lung 
and one to the left. The trachea may be on the left side of the 
oesophagus or behind it. 

INFLAMMATION. 

Acute Catarrhal Laryngitis. — This occurs as an idiopathic in- 
flammation, as a complication of the exanthemata and the infectious 
diseases, and is produced by the inhalation of irritating vapors and 
of hot steam and smoke. The inflammation varies in its intensity in 
different cases. The mucous membrane is at first congested, swol- 
len, and dry ; then the mucous glands become more active and an 
increased quantity of mucus is produced. There is an increase in 
the desquamation of the superficial epithelial cells and in the pro- 
duction of the deep cells. A few pus cells are found in the mucus 
and in the stroma of the mucous membrane. For some reason in- 
flammation of the larynx is frequently attended with spasm of its 



414 THE RESPIRATORY SYSTEM. 

muscles, thus producing attacks of suffocation. In severe cases 
oedema of the glottis may be developed. 

After death the congestion of the mucous membrane frequently 
disappears altogether. 

Chronic Catarrhal Laryngitis. — The surfacQ of the mucous 
membrane is dry or coated with muco-pus. The epithelium is thick- 
ened in some places, thinned in others, or in places entirely destroyed. 
The stroma is somewhat infiltrated with cells, diffusely thickened, or 
forming little papillary hypertrophies, or thinned, or necrotic and 
ulcerated (Fig. 198). 

The mucous glands are swollen and prominent. The inflamma- 




n 






Fig. 198.— An Ulcer of the Larynx in Chronic Catarrhal Laryngitis, x 850 and reduced. 

tion may extend to the perichondrium of the cartilages and thus 
cause their necrosis. The most severe forms of chronic laryngitis are 
those associated with pulmonary phthisis. Some forms of chronic 
laryngitis with thickening of epithelial and submucous tissue are 
called Pachydermia laryngis. 

Acute Suppurative Inflammation may attack the posterior sur- 
face of the epiglottis and the aryepiglottidean ligaments. The 
stroma of the mucous membrane is swollen and infiltrated with 
serum and pus. Abscesses may be formed in the stroma, which 
rupture internally, or extend outward into the neck, or into the wall 
of the pharynx or of the oesophagus. Suppurative inflammation 
may accompany catarrhal, croupous, tubercular, and syphilitic laryn- 



THE RESPIRATORY SYSTEM. 415 

gitis, inflammations and injuries of the pharynx and tonsils ; it may 
complicate typhoid fever and the other infectious diseases. 

Croupous Laryngitis occurs most frequently as one of the le- 
sions of diphtheria ; it complicates the exanthemata and the infec- 
tious diseases. It is produced by the Bacillus diphtheriae, by strep- 
tococci, by the inhalation of irritating gases, hot steam or smoke, 
and by the introduction of foreign. bodies. 

The mucous membrane is swollen and congested. Its surface is 
coated with fibrin and pus, and its stroma is infiltrated with fibrin 
and pus. The epithelial cells undergo coagulation necrosis. It is 
not often that there is necrosis of the deeper tissues. 




Fig. 199.— Tuberculous Laryngitis. 

Syphilitic Laryngitis. — Syphilis often causes laryngitis. The 
inflammation may have the ordinary characters of an acute or 
chronic catarrhal inflammation, or it is a productive inflammation 
w T ith the formation of new tissue in the stroma of the mucous mem- 
brane. This new tissue is principally composed of small cells, which 
often degenerate and die. In this way the mucous membrane of the 
larynx and the tissues beneath are thickened in some places and de- 
stroyed in others, these changes being especially marked in the upper 
portion of the larynx. If the perichondrium is involved by these 
changes there may be necrosis of the laryngeal cartilages. 

Tuberculous Laryngitis in its simplest form consists of a catarrhal 
inflammation, a growth of new cells in the stroma, and the forma- 



416 THE RESPIRATORY SYSTEM. 

tion of tubercle granula in the stroma without necrosis. The mu- 
cous membrane is thickened ; it is coated with a layer of mucus, 
pus, and desquamated epithelium. From the epithelial layer out- 
ward the stroma is infiltrated with cells and with tubercle granula 
(Fig. 199). 

When there are added to the production of tubercle tissue an ex- 
cessive formation of cells and a tendency to necrosis, the conditions 
become much more serious and complicated. The catarrhal inflam- 
mation is intense, with the production of large quantities of pus and 
mucus. The necrosis results in the formation of ulcers of different 
sizes and shapes ; the inflammation and necrosis extend from the 
mucous membrane to the wall of the larynx. The epiglottis, the 
vocal cords, and the adjacent mucous membrane are coated with 
muco-pus ; their surfaces are ragged and irregular. In places the 
mucous membrane is destroyed, so that ulcers are formed ; in places 
it is thickened and infiltrated with cells and tubercular tissue ; in 
places it is necrotic. In the most severe cases the entire thickness of 
the wall of the larynx, with its cartilages, is involved. 

CEdema of the Glottis is the name given to serous infiltrations 
of the mucous membrane of the upper part of the larynx. The 
swelling is most marked on the posterior wall of the epiglottis, in 
the aryepiglottidean ligaments and the false vocal cords. In these 
places the oedema of the stroma of the mucous membrane may be 
sufficient to close the larynx. 

Acute oedema is due to an inflammatory exudation of serum, and 
accompanies inflammations of the pharynx, larynx, and neck. 

Chronic oedema is of dropsical character and is caused by disease 
of the heart, pulmonary emphysema, and compression of the veins 
of the neck. 

TUMORS. 

Retention cysts of the mucous glands of the larynx may reach 
such a size as to form sacs projecting into its cavity. 

Papilloma is the most frequent form of tumor of the larynx. 
The tumors grow most frequently from the vocal cords. They con- 
sist of a connective-tissue stroma arranged so as to form papillae 
covered with epithelium. They are sometimes congenital. 

Fibromata, lipomata, myxomata, and angiomata are occa- 
sionally met with. 

Chondromata grow from the normal cartilages and are usually 
multiple and sessile. They may project into the cavity of the larynx. 

Sarcomata of the larynx have been seen in a considerable num- 
ber of cases. They occur both in children and in adults. They are 
composed of fusiform or round cells, with a stroma which varies in 
quantity in the different cases. 



THE RESPIRATORY SYSTEM. 417 

Carcinomata may invade the larynx from the tongue or the 
pharynx, or may originate in it. They are composed of flat epithelial 
cells packed together in the usual way. 

In the trachea tumors are of rare occurrence, but occasional 
examples of growths similar to those in the larynx have been met 
with. 

Cheesy and otherwise altered bronchial lymph nodes may by ul- 
cerative processes enter and obstruct the trachea. 

THE PLEURA. 
HYDROTHORAX. 

Non-inflammatory accumulations of clear serum in the pleural 
cavities are of frequent occurrence. They are produced by the 
same causes which effect dropsy in other parts of the body — le- 
sions of the heart, liver, and kidneys, and changes in the circulation 
and in the composition of the blood. 

If the amount of serum is small it is of little consequence ; if it 
is large it may compress the lower lobes of the lungs and interfere 
with respiration. 

There may be changes in the endothelium of the parietal pleura. 
Instead of the regular endothelium, large and small flat cells of ir- 
regular shape are found. 

HEMORRHAGE. 

Extravasations of blood in the substance of the pleura are found 
in persons who have died after suffering from the infectious dis- 
eases ; and as the result of injuries to the wall of the thorax. 

Blood in large quantity in the pleural cavities is found after rup- 
ture of an aneurism of the heart with rupture of the pericardium. 

Bloody serum in the pleural cavities is not often found with ordi- 
nary pleurisy. But with tubercular pleurisy and traumatic pleurisy 
it is not infrequently present. 

INFLAMMATION. 

The inflammations of the pleura are all spoken of by the common 
name of pleurisy, or pleuritis. 

All the different inflammations of the lung are capable of being 
accompanied by pleurisies, which begin in the pulmonary pleura 
and extend to the costal. 

Besides these, however, there are many pleurisies which belong 
primarily to the costal pleura and extend from there to the pulmo- 
nary pleura. 

Such pleurisies occur as idiopathic inflammations, as complica- 



418 THE RESPIRATORY SYSTEM. 

tions of various diseases, as the result of injuries, or are produced fr 
the inflammation of adjacent parts. 
We can distinguish : 

I. Pleurisy with the production of fibrin. 
II. Pleurisy with the production of fibrin and serum. 

III. Pleurisy with the production of fibrin, serum, and pus. 

IV. Chronic pleurisy with the formation of adhesions. 
V. Tuberculous pleurisy. 

All the varieties of pleurisy can best be studied in the lesion 
which are developed in and on the costal pleura. The lesions can b 
observed in the human subject, and can be produced artificially in th 
lower animals. It is in these artificial pleurisies especially that w 
are able to see the early changes produced by the inflammation am 
to watch the process step by step. 

The free surface of the costal pleura is covered with a single laye 
of flat cells — the endothelium. The pleura itself is formed of plane 
of connective tissue reinforced by elastic fibres. Connective-tissu 
cells with large bodies and branching processes are present in cor 
siderable numbers, being most abundant in the layers beneath th 
endothelium. In the connective tissue are embedded blood vessels 
lymphatics, and nerves. 

I. Pleurisy with the Production of Fibrin — Dry Pleurisy- 

Acute Pleurisy. 

This form of pleurisy is apt to involve circumscribed areas of th 
costal, mediastinal, diaphragmatic, or pulmonary pleura, less fre 
quently the entire pleura of one side of the chest. While th 
inflammation is going on the affected portion of pleura is coate 
with fibrin, the surface of the opposite portion of pleura is coated i 
the same way, and bands of fibrin join the two together. After th 
inflammation has run its course we find the affected portion of pleur 
thickened by the formation of new connective tissue, while bands c 
connective tissue extend between the opposed pleural surfaces. 

As an exceptional condition there is inflammation of the entir 
pleura of one side, with the production of such an enormous amour 
of fibrin as to compress the lung and cause death. 

II. Pleurisy with the Production of Fibrin and Serum — Pleuris 

with Effusion — Subacute Pleurisy. 

This is the most common form of pleurisy. As a rule, it involve 
the greater part of the pleura of one side of the chest. Sometime!: 
however, the pleura of both sides of the chest is involved, and the 
the pericardium also is often inflamed. 



THE RESPIRATORY SYSTEM. 419 

While the inflammation is in progress the surface of the affected 
pleura is coated with fibrin, and bands of fibrin stretch between the 
parietal and pulmonary pleura. In the pleural cavity is serum in 
variable quantity. This serum is clear, or turbid from the presence 
of pus cells and flocculi of fibrin. The lung is compressed in different 
degrees and positions, according to the quantity of the serum and 
the character of the adhesions. 

If the patient recover the serum is absorbed, the fibrin disappears, 
and there are left behind connective-tissue thickenings of the pleura 
and adhesions. 

These two forms of pleurisy, although different in their clinical 
histories, are yet anatomically essentially the same. In both of 
them we find a regular sequence of changes. First, the production 
of fibrin and a few pus cells, either with or without serum. Second, 
a gradual absorption of the serum and fibrin. Lastly, the formation 
of permanent new connective tissue in the form of adhesions or of 
thickenings of the pleura. Throughout the whole process the tissue 
of the pleura is but little changed ; the products of inflammation, 
although they originate in the tissue of the pleura, do not infiltrate 
it, but make their way to its surface, there accumulate, and there 
undergo their different changes. Variations from the regular course 
of the inflammation are effected by the excessive formation either of 
the fibrin, the pus, or the serum, and by the manner in which these 
inflammatory products are absorbed. 

If we endeavor to follow out the successive changes by which the 
fibrin, pus, and serum make their appearance and then disappear, 
and the way in which permanent new connective tissue takes their 
place, we encounter several difficulties. It is difficult to obtain 
autopsies which will give the lesions belonging to each successive 
day of the disease ; the pleura does not really show well if the pa- 
tient has been dead more than two or three hours before the autopsy; 
and in most cases the inflammation is too intense, its products are 
too abundant, to be easily studied. 

To obviate these difficulties we must resort to experiments on the 
lower animals. By injecting a solution of chlorid of zinc into the 
pleural cavities of dogs we can excite pleurisies closely resembling 
those which we see in the human subject. By varying the amount 
of fluid injected we can obtain pleurisies of different degrees of 
intensity. By using a number of animals we can observe the course 
of the inflammation from hour to hour and from day to day. 

In such an artificial pleurisy the first change is congestion. The 
pleura is of a uniform bright-red color, its surface moist and shining. 
There is as yet no serum and no fibrin. Already, however, the en- 
dothelial cells have fallen off in patches, the superficial connective- 



420 



THE RESPIRATORY SYSTEM. 



tissue cells are swollen and increased in number, and a few pus 
cells are present. These are all the changes for from half an hour to 
six hours after the irritant has been applied to the pleura. 

The next step in the inflammatory process is the production of 
serum and fibrin. The serum collects in the bottom of the pleural 
cavity, the fibrin coats the pleura. As the fibrin is produced the 
pleura loses its natural moist and shining appearance. The fibrin 
appears first in the form of little granules, knobs, and threads be- 
tween the edges of the endothelial cells and overlying them. A few 
pus cells are entangled in the fibrin and infiltrated in the superficial 
layers of the pleura. The swelling and new growth of the connec- 



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Fig. 200.— An Artificial Pleurisy in the Dog, of Twenty-four Hours 1 Duration, x 75( 
and reduced. . 

Swelling and growth of connective-tissue cells in the pleura. 



tive-tissue cells are now well marked. The bodies of the branching 
cells are swollen, and small polygonal, nucleated cells, arranged in 
rows between the fibres of the basement substance, make their ap- 
pearance. By the end of twenty-four hours these changes are fully 
developed (Fig. 200). 

After this the production of fibrin, serum, and new connective- 
tissue cells continues, and by the third or fourth day the new connec- 
tive-tissue cells are present, not only in the superficial layers of the 
pleura, but also in the layer of fibrin coating its surface and forming 
adhesions. 

By the fourth or fifth day the cells in the fibrin are still more 



THE RESPIRATORY SYSTEM. 421 

numerous ; blood vessels make their appearance, which can be in- 
jected from the arteries of the pleura. 

After this the serum is gradually absorbed. The layer of fibrin 
and cells on the surface of the pleura exhibits a constant decrease of 
fibrin and increase of cells, and becomes more intimately connected 
with the surface of the pleura. 

By the fourteenth day the fibrin has disappeared and a basement 
substance has been formed between the cells. Of the new cells the 
superficial ones are changed into endothelium, the deeper ones into 
branching cells. The changes in the adhesions between the pulmo- 
nary and costal pleura are the same as those in the layer of fibrin 
coating the costal pleura. 

The lesions of human pleurisy seem to be essentially the same as 
those of the artificial pleurisy just described. But the inflammatory 
products are formed in larger quantities, a much longer time is re- 
quired for their absorption, and the formation of new connective 
tissue follows more slowly. 

In these forms of pleurisy, therefore, two distinct processes take 
place : 

1. The blood vessels are congested, and through their walls trans- 
ude the plasma of the blood and a few white blood globules. 

2. The superficial connective-tissue cells are increased in size and 
number. 

The products of the first of these processes, the fibrin and serum, 
are regularly reabsorbed. 

The product of the second of these processes, the new connective- 
tissue cells, regularly increases until a layer of new connective tissue 
is formed. 

The natural termination of such a pleurisy is the recovery of the 
patient, with thickenings of the pleura and adhesions. 

The irregular terminations are : The death of the patient, the 
protracted existence of the fibrin and serum, and the change of the 
character of the inflammation so that pus is produced. 

In a considerable proportion of cases the examination of the exu- 
date in a simple uncomplicated case of sero-fibrous pleurisy fails to 
reveal the presence of micro-organisms. 

III. Pleurisy with the Production of Fibrin, Serum, and Pus — 

Empyema. 

This form of pleurisy may occur under several different condi- 
tions. 

1. The inflammation is at the very outset of severe character, 
with the formation of pus. 



422 THE RESPIRATORY SYSTEM. 

2. A pleurisy with the production of fibrin and serum, either 
gradually or suddenly, changes its character and pus is formed. 

3. Phthisical areas of softening, or abscesses of the lung, abscesses 
in the wall of the thorax, or in the liver, or in the abdomen, rupture 
into a pleural cavity and set up an empyema. 

4. The inflammation may be not only purulent but also gangre- 
nous in character. The fluid in the pleural cavity, the fibrin and 
pus coating the pleura, and the pleura itself, may putrefy, with the 
proliferation of bacteria and the evolution of gases. This may take 
place either in a closed pleura or in one which has been opened. 

5. If there is an opening into a pleural cavity, either through the 
lung or through the wall of the thorax, there is air in the pleural 
cavity, in addition to the inflammatory products. Such a condition 
is called pyo-pneumothorax. 

In all these different cases the pleural cavity is partly or com- 
pletely filled with purulent fluid, and the lung is either compressed 
against the vertebral column or partly adherent to the chest wall. 
Sometimes, however, the purulent fluid is shut in by adhesions, 
either between parts of the lung and the thoracic wall, or between 
the lung and the diaphragm, or between the lung and the pericar- 
dium, or between the lobes of the lung. 

The fluid in the pleural cavity is usually a thin, purulent serum, 
composed of serum, pus globules, endothelial cells, and pieces of 
fibrin. But sometimes this fluid is very thick and viscid. 

In empyema in its earlier stages the lesions are the same as 
those in pleurisy with effusion, with the addition of pus in the serum, 
the fibrin, and the superficial layers of the pleura. 

In children the inflammation may remain in this condition for a 
long time, but in adults other changes in the pleura are soon devel- 
oped. 

These changes consist in the growth of a large number of small 
polygonal and round cells, the basement substance is split up, and 
the pleura is changed into a tissue resembling granulation tissue. 

The pleura is thus considerably thickened. Its surface is coated 
with fibrin and pus, or is bare like the surface of an ulcer. 

In this condition the pleura may remain for months or years, 
its inner layers formed of granulation tissue, its outer layers of dense 
connective tissue. 

Sometimes the cell growth is more active, necrotic changes are 
added, and so there is a conversion of portions of the pleura into 
pus. Such a suppuration may extend from the pleura to the fas- 
ciae, the muscles, the skin, the diaphragm, or the lungs. Thus the 
pus may find an exit, through the wall of the thorax, into the peri- 
toneal cavity or into the lungs. 



THE RESPIRATORY SYSTEM. 423 

If the empyema becomes gangrenous the pleural cavity contains 
foul gases, the purulent serum is dirty and stinking and swarms with 
bacteria. The fibrin coating the pleura is of green or brown color. 
Portions of the pleura itself may also become gangrenous. 

In old cases the thickening of the pleura may reach an enormous 
degree and it may become calcified. 1 The perichondrium of the car- 
tilages and the periosteum of the ribs may become inflamed, with ne- 
crosis of the cartilages and ribs or a production of new bone. 

Empyema is, therefore, a very much more serious lesion than 
the two forms of pleurisy just described. The lesions involve not 
merely the surface of the pleura, but its entire thickness. When the 
pleura has thus been converted into granulation tissue it is hardly 
possible for it to return to a normal condition. 

It is important to remember that in children the changes in the 
pleura itself are less profound, and that in adults they become more 
and more marked, according to the duration of the disease. 

Bacteria 2 are present in the exudate in a large proportion of cases 
of empyema. The Streptococcus pyogenes, Staphylococcus pyogenes, 
Diplococcus lanceolatus, and the Bacillus tuberculosis are the most 
common inciters of suppurative inflammation of the pleura. 

Interlobular Lymphangitis. — Inflammations of the pleura with 
the production of pus and fibrin may extend to the lymphatics in the 
interlobular septa, around the bronchi, and around the blood vessels. 
This occurs with pleurisies due to septic poisoning and with those 
which occur without discoverable cause. It is seen more frequently 
in children than in adults. The lymphatics in the interlobular septa, 
and those around the bronchi and blood vessels are distended with 
pus cells, the septa are much thickened, and the lobules separated 
from each other. 

IV. Chronic Pleurisy with the Formation of Adhesions. 

This form of pleurisy may follow one of the varieties of pleurisy 
just described, it may be associated with emphysema and chronic 
phthisis, or it may occur by itself. 

After death the pulmonary and costal pleura are found thickened 
and joined together by numerous adhesions. These changes may 
involve only a part or the whole of the pleura on one or both sides 
of the chest. 



1 For a resume of our knowledge of various calcifications in the lungs, and allied 
conditions olten called "lung stones," consult Polaillon, "LesPierres du Poumon,'' 
etc., Paris, 1891 ; or Legry, Arch, gen.de Med., March and April, 1892. 

2 Consult "iEtiology of Exudative Pleuritis, " Prudden, New York Medical Jour- 
nal, June 24th, 1893. On the relationship between empysema and subphrenic ab- 
scess, consult Meltzer, New York Medical Journal, June 24th, 1893. 



424 THE RESPIRATORY SYSTEM. 

The thickened pleura is covered with endothelial cells, which are 
increased in size and number ; the connective-tissue cells in the 
pleura are also increased in number, and the blood vessels are more 
numerous. 

The adhesions are formed of connective tissue resembling that of 
the costal pleura, containing blood vessels and covered with endo- 
thelium. 

V. Tuberculous Pleurisy. 

In acute general tuberculosis miliary tubercles are often preseni 
in the pleura. In acute and chronic phthisis, besides the fibrin, pus. 
serum, and new connective tissue so often produced, there may alsc 
be miliary tubercles or larger, flat, cheesy nodules. 

There are, however, cases of tuberculous pleurisy which have thi 
characters of a local tubercular inflammation. Tubercles are eithei 
absent altogether from the rest of the body or of secondary import- 
ance to the pleurisy. 

This form of pleurisy involves the pleura of one side of the tho- 
rax only. It may be rapidly developed, the patient dying at the end 
of two weeks ; or it may continue for months. It seems to be verj 
fatal. 

The inflammation may be confined to the costal pleura or may in- 
volve also the diaphragmatic and pulmonary pleura. The gross ap- 
pearance of the lesion varies. 

1. The pleura is thickened, its surface is bare of fibrin ; it is of s 
bright-red color from the congestion of the blood vessels, and this rec 
surface is mottled with white dots — the miliary tubercles. In the 
pleural cavity is bloody serum. 

2. The pleura is thickened ; it is thickly coated with fibrin ; nc 
tubercles are visible to the naked eye ; the pleural cavity contains 
clear serum. 

3. The pleura is thickened and the pleural cavity contains puru 
lent serum. 

In all the cases the changes in the pleura itself are essentially th« 
same. The thickened pleura is infiltrated with new connective-tissu 
cells. Scattered through its entire thickness are tubercle granula 
either single or joined together by diffuse tubercle tissue (Fig. 201) 
The smaller blood vessels show a growth of their endothelial cells. 

In the exudate of tuberculous pleuritis the tubercle bacillus ma^ 
frequently be detected by simple staining, especially if the solid ele 
ments be brought together from a considerable quantity of the fluic 
by a centrifugal machine. 

But in suspicious cases of exudative pleurisy which give nega 
tive results on morphological examination of the fluid, the inocula 



THE RESPIRATORY SYSTEM. 



425 



tion of guinea-pig with a considerable amount of the exudate or with 
the material concentrated by the centrifuge is more decisive and may 
reveal the nature of the lesion when the simple morphological tests 
have failed. 

TUMORS. 

Fibroma. — Little white or pigmented fibromata, of the size of a 
pin's head and scarcely raised above the surface, are often present in 
the pulmonary pleura. 




Fig. 211.— Tcbrrcclous Pleurisy. X 90 and reduced 
Drawn from a vertical section of the costal pleura. 



Larger fibrous tumors are formed in the deeper layers of the cos- 
tal pleura, and project into the pleural cavity. They may become de- 
tached and are then found loose in the pleural cavity (Lebert). 

Lipoma. — Fatty tumors are formed beneath the costal pleura 
and project into* the pleural cavitv (Lebert). 



426 THE RESPIRATORY SYSTEM. 

Carcinomata, sarcomata, and lymphomata are usually second- 
ary to similar tumors in other parts of the body. 1 

A peculiar form of primary new growth in the pleura has been 
described by several observers. 2 It is associated with a pleurisy with 
the production of fibrin and serum. There is a diffuse thickening of 
the costal pleura, or circumscribed nodules of different sizes. 

The new growth seems to begin in the lymphatics of the pleura, 
which are distended with flat, nucleated cells. 

I (Delafield) have seen two of these cases. The first case was a 
woman, fifty-three years old, who was ill, with the symptoms of 
pleurisy with effusion, for four months. After death the left pleural 
cavity was found to be full of bloody, purulent serum. The costal 
pleura was moderately thickened and coated with a layer of fibrin 
and pus. Beneath the fibrin and pus was a thin layer of granula- 
tion tissue. In this tissue and in the pleura were anastomosing tu- 
bules filled with flat, nucleated cells. The tubules looked like lym- 
phatics. 

The second case was a man, sixty-three years old, who had symp- 
toms of pleurisy with effusion, for four months. After death the 
right pleural cavity was found half -full of bloody serum. The cos- 
tal, diaphragmatic, and pulmonary pleura were coated with fibrin 
and contained numerous white nodules, some of them as large as a 
pigeon's egg. These nodules were formed of a connective-tissue 
stroma enclosing irregular spaces and tubules filled with flat, nu- 
cleated cells. 

While these tumors are often puzzling, and the observer may be in 
doubt whether they should be called endothelioma or carcinoma or 
sarcoma, recent studies seem to indicate that they are, for the mosi 
part at least, endotheliomata (see page 312). 

THE BRONCHI. 
INFLAMMATION. 

Acute Catarrhal Bronchitis is a disease of very common occur- 
rence, but one which seldom proves fatal. Our knowledge of its 
lesions is derived from severe cases, from experiments on animals, 
from cases which are complicated by other diseases, and from the 
symptoms which we observe during life. 

The inflammation involves regularly the trachea and the larger 
and medium-sized bronchi, less frequently the smaller bronchi also. 
As a rule, the bronchi in both lungs are equally affected. 

1 For description of ciliated cysts of the pleura, consult Zahn, referred on p. 543. 

2 Birsch-Hirschfeld, "Path. Anat., " p. 768. E. Wagner, Arch. d. Heilkunde, xi. 
B. Schulz, Arch. d. Heilkunde, xv. Ihierfelder, "Atl. d. path. Hist.," 4 Lief. 
Frdnkeh Berliner klin. Wochenschrift, May 23d, 1892. 



THE RESPIRATORY SYSTEM. 427 

The first change seems to consist in a congestion and swelling of 
the mucous membrane, with an arrest of the functions of the mucous 
glands* This is attended with pain over the chest, a feeling of op- 
pression, sometimes spasmodic dyspnoea, and a dry cough. After 
this the mucous glands resume their functions with increased activity, 
the congestion diminishes, there is an increased desquamation of epi- 
thelium, an increased formation of the deeper epithelial cells, and a 
moderate emigration of white blood cells. Sometimes the red blood 
cells also escape from the vessels. The patient now has less pain and 
oppression ; the cough is accompanied with an expectoration of mu- 
cus mixed with epithelium, pus, and sometimes blood. 





Fig. 202.— Acute Catarrhal Bronchitis, x 850 and reduced. 



After death the only lesions visible are the increased amount of 
mucus, the growth of new epithelium, mucous degeneration of the 
epithelial cells, a few pus cells infiltrating the stroma, and the gene- 
ral congestion of the mucous membrane. The whole process is a 
superficial one, not producing any changes in the walls of the bron- 
chi beneath the mucous membrane (Fig. 202). 

When the inflammation involves the smaller bronchi also they 
may be full of pus, but their walls are unchanged. 

The filling of the small bronchi may result in the collapse of the 
groups of air vesicles to which they lead, and thus are produced areas 
of atelectasis^ which may be further changed by inflammatory pro- 
cesses. 



428 



THE RESPIRATORY SYSTEM. 



Chronic Catarrhal Bronchitis. — This form of bronchitis nig 
be the sequel of one or more attacks of acute bronchitis. More fr 
quently it is associated with emphysema, heart disease, interstiti 
pneumonia, phthisis, pleuritic adhesions, or the inhalation of irrita 
ing substances. 

There is in most cases a constant production of mucus, pus, ai 
serum in considerable quantities, and these inflammatory produc 
may have a very foul odor. Less frequently these products are ve: 
scanty — dry catarrh. 




Fig. 203.— Croupous (Fibrinous) Bronchitis. 
Fibrinous casts of the bronchi, similar to those shown in the photographs, were coughed 
at irregular intervals for several years. 



In examining the bronchi in these cases after death we are oft< 
struck by the want of proportion between the symptoms and tl 
lesions. The same bronchi which during life were constantly pi 
ducing large quantities of inflammatory products and injuring t' 
patient's health, after death may be but little changed from the nc 
mal. In other cases, however, the lesions are more marked. 

The bronchi contain mucus and pus ; they may be congestec 
their walls are often trabeculated. The epithelium is deformed ai 
desquamating, with a production of new cells in the deeper layei 



THE RESPIRATORY SYSTEM. 429 

the mucous glands are large or atrophied. The connective- tissue 
stroma is thickened and infiltrated with cells. The coats of the ar- 
teries in the walls of the bronchi may be thickened. There may be 
cylindrical dilatation of one or more bronchi. The muscular coat 
may be thickened or thinned. Very frequently the epithelial cells 
of the air vesicles and air passages are increased in size and number. 

Acute Croupous Bronchitis occurs as a lesion of diphtheria, as 
associated with croupous laryngitis, as the result of the inhalation of 
hot steam, with lobar pneumonia, and sometimes as an idiopathic 
disease. 

The bronchi are lined or filled with a mass of fibrin, pus, and de- 
squamated epithelium. Fibrin and pus may also be found beneath 
the epithelium and infiltrated in the stroma. 

Chronic Croupous Bronchitis is attended with the formation in 
one or more bronchi of masses of fibrin which are expectorated by 
the patient in the form of branching casts of the bronchi (Fig. 203). 
The disease is a very chronic one, and is often associated with 
phthisis. After death the bronchi are said to be found but little 
altered from the normal. 

Curschmann 1 has described under the name of "bronchiolitis 
exudativa " sl form of bronchitis in which small threads and bands of 
gray or yellow, partly transparent, coagulated matter are formed in 
the small bronchi. Vierordt 2 has found similar formations in lobar 
pneumonia. Leyden and Levi have found them in broncno-pneu- 
monia. 

In different forms of bronchitis, especially in those associated 
with asthma, the exudation may contain small, octahedral bodies, 
probably composed of mucin. They are accidental formations, prob- 
ably formed from cells, and may be found in the sputa. 

BRONCHIECTASIA. 

Dilatation of the bronchi presents itself under three forms : the 
cylindrical, the fusiform, and the sacculated. 

The cylindrical dilatation is a uniform enlargement of one or more 
bronchi for a considerable part of their length. It is found in 
bronchi of every size, but most frequently in the medium-sized. 

The fusiform dilatation is a mere variety of the cylindrical. The 
bronchus is uniformly dilated for a short distance, and then resumes 
its natural size. Several such dilatations may be found in the same 
bronchus. 

Tlie sacculated dilatations form the largest cavities. These cavi- 

J Deutsch. Arch. f. klin. Med., xxxii. 

2 Berl. klin. Wochensch., 1883. B. Levi, Zeitsch. f. klin. Med., ix. Leyden, 
Virch. Arch., Bd. lxxiv. 



430 



THE RESPIRATORY SYSTEM. 



ties communicate with one side of the bronchus; the peripneral por- 
tion of the bronchus may be obliterated. The bronchus leading to 
the cavity may be of normal size, or dilated, or stenosed, or even 
completely obliterated. Such sacculated dilatations may reach a 
very large size and may communicate with each other. 

Any inflammatory process which involves the thickness of the 
wall of a bronchus seems to be capable of producing dilatation of that 
bronchus. 

In acute general bronchitis and broncho-pneumonia in children, 
cylindrical dilatation of a number of the medium-sized bronchi is 
often produced. 



Fig. 204-— Section of the Wall of a Bronchiectasia, x 850 and reduced. 



In the persistent broncho-pneumonia of children such dilatations 
reach a still greater development. 

In acute and chronic phthisis tubercular inflammation gives rise 
to sacculated dilatations, which expand with time and are made 
still larger by the destruction of the adjacent lung tissue. 

Chronic bronchitis may lead to cylindrical or sacculated dilata- 
tions, sometimes of great size. 

Occlusion of some of the bronchi, consolidation of portions of the 
lung, and extensive pleuritic adhesions, may also produce bronchi- 
ectasia. 



THE RESPIRATORY SYSTEM. 431 

The walls of these dilatations may preserve the characters of the 
wall of the bronchus, more or less altered by inflammation (Fig. 
201), or these characters may be altogether lost. The dilatations 
may contain mucus and pus, or they may be empty. 

TUMORS. 

Ossification of the walls of the bronchi is sometimes found. 

Lipoma in the submucous connective tissue has been described 
by Rokitansky. Fibroma and chondroma have been described. 

Sarcomata of the walls of the bronchi occur as secondary growths, 
and as extensions of similar growths in the mediastinum. Primary 





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Fig. 205. — Adenoma op the Bronchi. 
From a specimen loaned by Dr. Stewart. 

sarcoma of the bronchi 1 seems to be rare. Hesse describes a form of 
lympho-sarcoma forming nodules around the bronchi as of common 
occurrence among the miners in some cobalt and nickel mines. 

Adenoma of the bronchi is of rare occurrence (Fig. 205). 

Primcwy carcinoma of the bronchi is described by several 
authors, but it is not common. 

Langhans describes a primary carcinoma of the lower end of the 
trachea and the large bronchi in a man forty years old. The lower 
end of the trachea and the large bronchi showed a general thickening 
of their walls, with flat tumors projecting inward. The new growth 

1 Hesse, Archiv d. Heilkunde, xix. , p. 160. 



432 THE RESPIRATORY SYSTEM. 

was composed of a stroma enclosing cavities rilled with cells. The 
cells were small, nucleated, polygonal or cylindrical in shape, and 
packed closely together. Apparently the new growth originated in 
the mucous glands. 

Carcinoma of the walls of the bronchi may occur as a secondary 
lesion. It may be formed in the large or small bronchi, follow the 
course of the bronchial tree, or extend to the lung tissue or to the 
trachea. 

THE LUNGS. 
MALFORMATIONS. 

One or both lungs may be entirety wanting or only partially de- 
veloped. In some of the cases with only one lung the patients havp 
grown up to adult life. 

A peculiar degeneration, by which the lung is converted into a 
number of sacs containing air and serum, the sacs communicating 
with the bronchi, has been seen in a few instances. 

The lobes may be subdivided by deep fissures. An accessory lobe, 
separated from the lung, between the base of the left lung and the 
diaphragm, has been described by Rokitansky. 

There may be hernia of the lung, with absence of part of the wall 
of the thorax. 

There may be transposition of the lungs, with similar changes in 
the position of the heart and the abdominal viscera. 

INJURIES — PERFORATIONS. 

Severe contusions of the thorax may produce rupture of the lungs, 
with extravasations of blood into the pleural cavities. 

The lungs may be wounded by a fractured rib and by penetrating 
weapons and projectiles. Such injuries often produce bleeding into 
the lung tissue and inflammatory changes. The lungs, however, 
exhibit a considerable degree of tolerance for such injuries, and the 
patients often recover. 

Collections of pus in the pleural cavities, the mediastinum, the 
liver, the spleen, the kidneys, and the peritonal cavity may perforate 
the lungs. Abscess of the lung may be secondary to liver abscess 
from amoeba coli. 

CONGESTION AND CEDEMA. 

These two conditions are regularly associated with each other in 
the lungs, although one or the other of them may preponderate in 
ditferent cases. 



THE RESPIRATORY SYSTEM. 433 

A moderate degree of congestion and oedema of the posterior por- 
tions of the lungs is often found as a result of post-mortem changes. 

In persons who have been comatose from any cause for some 
hours before death, congestion and oedema of the lungs are regularly 
developed. 

With disease of the heart, kidneys, and lungs the congestion, and 
especially the oedema, may be excessive. The lungs may be so com- 
pletely infiltrated with serum as to be unaerated. Such a solid 
oedema of the lungs is sufficient of itself to cause death. It has been 
asserted by Welch 1 that the cause of such an excessive oedema is a 
paralysis of the left side of the heart, while the force of the right 
heart is unimpaired. Such an explanation seems to be plausible. 2 

Patients confined to bed for a considerable length of time may 
develop congestion of the dependent portions of the lungs — hypo- 
static congestion. The affected portion of lung is shrunken, con- 
gested, and imperfectly aerated. 

HEMORRHAGE. 

Extravasations of blood within the air cavities are found with the 
general diseases which produce a disposition to bleeding in different 
parts of the body. 

Blood from the bronchi or from cavities may be inspired into the 
air vesicles. 

Valvular lesions of the heart, especially of the mitral valve, are 
often accompanied by the production of hsemorrhagic infarctions in 
the lungs. These infarctions are circumscribed, of rounded or wedge- 
shaped forms, from the size of a walnut to that of an orange. They 
are of dark-red color, unaerated, the air passages distended with 
blood, and are often surrounded by a zone of pneumonia. They may 
be situated in any part of the lungs, but are most common in the 
lower lobes. When they are near the surface of the lungs a circum- 
scribed pleurisy is often produced. 

Such infarctions may produce death; they may become gangre- 
nous, or the blood may become absorbed, or they may be gradually 
changed into a smaller mass of pigmented fibrous tissue. 

These infarctions are usually produced by emboli or by thrombosis 
of branches of the pulmonary artery. 

Infarctions of smaller size, and with more disposition to be sur- 
rounded by inflammatory changes, are produced by emboli from the 
right side of the heart and from thrombi in the veins of pysemic 

1 Virchow's Archiv, Bd. 72. 

2 For bibliography, etc., of pulmonary oedema consult Lowit, Ziegler's Beitrage 
zur path. Anat., etc., Bd. xiv., p. 401, 1893. 



434 THE RESPIRATORY SYSTEM. 

patients. These infarctions are usually situated near the surface oJ 
the lung. 1 

Haemorrhages with rupture of the lung tissue are produced 03 
severe contusions, by penetrating wounds, and by the rupture o: 
aneurisms. 

EMPHYSEMA. 

Emphysema is of two kinds — interlobular and vesicular. 

Interlobular Emphysema is produced by the rupture of air spa 
ces and the escape of air into the interstitial tissue of the lung 
Or the pulmonary pleura may also be ruptured and the air escap< 
into the pleural cavity, or into the mediastinum and from thence int< 
the neck. Such a rupture of the air spaces is most frequently causec 
by broncho-pneumonia with consolidation of portions of the lungs. 

Vesicular Emphysema is a dilatation of the air passages and vesi 
cles of the lungs. A temporary emphysema can be produced in 1 
variety of ways. The bronchi may be obstructed in such a way tha 
the air can enter the air spaces, but cannot escape from them. A 
portion of the lungs may be consolidated or compressed, and thei 
the air spaces of the rest of the lungs will be dilated. Death ma] 
take place, with a dilatation of the lungs which remains after death 

Permanent emphysema may change an entire lung if the othe: 
lung becomes permanently unaerated ; it may change portions of i 
lung if other portions are consolidated. 

"Substantive emphysema" is a term which is now used in £ 
clinical rather than in an anatomical sense. It is used to designat* 
a group of cases in which there are regularly developed changes ir 
the shape of the thorax, certain characteristic physical signs, a lia 
bility to bronchitis, to constant and spasmodic dyspnoea, to venous 
congestion of the viscera and of the skin. In patients who presen' 
such symptoms during life, we find after death diffuse changes oJ 
both lungs, of which dilatation of the air spaces may form a pari 
(Fig. 206). If the dilatation of the air spaces does exist, the tern: 
"substantive emphysema" is appropriate; if it does not exist wt 
employ a term which contradicts itself. 

The real lesion of substantive emphysema is a chronic productive 
inflammation of the lung with the formation of new connective tis- 
sue — a process analogous to similar chronic inflammations of the en 
docardium, arteries, and kidneys, and one which, like them, ma} 
constitute a formidable disease or an unimportant senile change. 

Both lungs are moderately or considerably increased in size. Verj 
often they are partly covered by connective-tissue pleuritic adhesions. 



1 Recent studies on lung infarctions have been made by Grawitz, "Festschrift' 
for Virchow's 71st birthday, 1891. 



THE RESPIRATORY SYSTEM. 



435 



The mucous membrane of the bronchi may be coated with mucus or 
with muco-pus. The muscular coat of the bronchi may be thick- 
ened ; their entire wall may be thickened or thinned and infiltrated 
with cells ; they may be narrowed or dilated ; they may be sur- 
rounded by zones of pneumonia. The cells which line the walls of 




Fig. 206.— Pulmonary Substantive Emphysema. 
Blood vessels injected, showing dilatation of the air spaces and new growth of interstitial 
connective tissue. 

the air spaces are increased in size and number. The walls of the 
air spaces are more or less thickened, except in the case of some of 
the air spaces which are dilated. In the walls of some of the air 
spaces, those which are thickened as well as those which are thinned, 
are formed small holes (Fig. 207) which may later reach a' large 
size, so that adjacent air spaces become fused together. ' 

In some cases of substantive emphysema no dilatation of the air 
spaces exists. ' In many of the fatal cases the dilatation is but 
moderate ; in some cases it is very marked. The dilatation may 



436 



THE RESPIRATORY SYSTEM. 



involve the air passages alone, or both the air passages and th( 
vesicles. It is not uniform, but involves some parts of the lungs 
more than others. 

The arteries throughout the lungs and in the walls of the large] 
bronchi may have their coats thickened. The capillaries in th< 
walls of the air spaces which are but little dilated are unchanged 
Those of the dilated air spaces are separated by wider intervals 
they may be smaller ; it is said that they may be obliterated. 

The right ventricle of the heart may be dilated or hypertrophied 
or both. There may be venous congestion of the pia mater, th< 



"^SiT^r?7^~~T^?r^ 




. . *-/ 



Fig. 207.— Emphysema, showing Holes in the Walls of the Air Vesicles, X 850 and reduced. 
From a case of chronic miliary tuberculosis. 

stomach, the small intestine, the liver, the spleen, the kidneys, and 
the skin. There may be dropsy. 



ATELECTASIS. 



A collapsed and unaerated condition of portions of lung tissue is 
either congenital or acquired. 

1. In congenital atelectasis portions of the lung are firm, non- 
crepitant, of a dark-blue or purple color, depressed and smooth on 
section. These portions can usually be artificially inflated, and then 



THE RESPIRATORY SYSTEM. 437 

cannot be distinguished from the surrounding pulmonary tissue. 
This condition is produced by the inability of the child after birth to 
fully inflate its lungs, either from want of sufficient vitality or from 
obstruction of the bronchi. If the child lives for some time, and the 
collapsed lobules are not inflated, they become hard and dense. 

2. In young children the smaller bronchi may become ob- 
structed by the inflammatory products of bronchitis and the corre- 
sponding air vesicles will then collapse. We then find scattered 
through the lungs collapsed lobules like those in the new-born child. 
Inflammatory changes may be subsequently developed in the col- 
lapsed lobules. 

3. In adults, large or small portions of lung tissue may become 
collapsed as the result of bronchitis, of stenosis of a large bronchus, 
of compression of a bronchus, of paralysis of the pneumogastric, of 
compression of the lungs by fluid or by new growths, and of long- 
continued feebleness of the act of respiration. 



GANGRENE OF THE LUNGS. 

It is customary to distinguish two forms of gangrene of the lung, 
the circumscribed and the diffuse ; yet both can occur together. 

Circumscribed gangrene occurs in the form of one or more 
rounded or irregular masses of variable size. The gangrenous por- 
tion of lung is at first brown and dry. The surrounding lung tissue 
is congested or cedematous, or infiltrated with blood, or inflamed. 
If the gangrenous focus is near the pleura the latter will be coated 
with fibrin. Gradually the gangrenous portion of lung assumes a 
dirty-green color and a putrid odor. It becomes soft, broken down, 
and separated from the surrounding lung. The blood vessels may 
be obliterated by thrombi, or eroded, so that there are profuse haemor- 
rhages. 

Such a gangrenous process may extend to the adjacent lung 
tissue, or a zone of gray or red hepatization or of connective tissue 
may be formed. 

The fluid from the gangrenous lung may pass into the bronchi 
and be expectorated; or it may run from one bronchus into another 
and set up new gangrenous foci or diffuse gangrene. 

The pulmonary pleura may be perforated and a gangrenous pleur- 
isy produced. Gangrene may follow lobar or broncho-pneumonia, 
especially such phases of the latter as result from the inspiration of 
foreign material containing micro-organisms from the mouth ; it may 
arise from infectious emboli in the lungs, or by an extension of a gan- 
grenous process from an adjacent part. 

Diffuse gangrene may follow the circumscribed form; it may 






438 THE RESPIRATORY SYSTEM. 

complicate lobar pneumonia or occur as an idiopathic condition. A 
large part of a lobe or of an entire lung becomes greenish, putrid, 
and soft, and the pulmonary pleura is inflamed. There may be haem- 
orrhages from eroded vessels. There may be general septicaemia. 

Various forms of bacteria may be present in gangrenous areas of 
the lungs. Among those frequently present is the Staphylococcus 
pyogenes, Streptococcus pyogenes, pneumococcus, and various sapro- 
phytic micro-organisms. 



PNEUMONIA. 

The inflammations of the lungs, as distinguished from those of 
the bronchi and pleura, are called "pneumonia." 

In the present state of our knowledge the classification of the 
different forms of pneumonia must be an arbitrary one. We describe 
separately : 

I. Acute lobar pneumonia. 
II. Broncho-pneumonia. 

III. Secondary and complicating pneumonia. 

IV. The pneumonia of heart disease. 
V. Interstitial pneumonia. 

VI. Tuber ctdous pneumonia. 
VII. Syphilitic pneumonia. 

I. Acute Lobar Pneumonia. 

This is an acute exudative inflammation, which involves regularly 
the whole of one lobe, or the larger part of one lung, or portions of 
both lungs. It is an infectious inflammation, caused by the growth 
in the lung of the Diplococcus lanceolatus (Diplococcus pneumoniae 
of Frankel) (see page 201). * 

The inflammation is of pure exudative type, characterized by con- 
gestion, emigration of white blood cells, diapedesis of red blood cells, 
and exudation of blood plasma, while the tissue of the lung itself is 
but little changed. 

During the first hours of the inflammation, only irregular por- 
tions of the lobe which is to be inflamed are involved ; later the entire 
lobe. The lung is congested, oedematous, tough, but not consoli- 
dated. The air spaces contain granular matter, fibrin, pus cells, red 

1 There are occasional irregular forms of pneumonia attended with the growth of 
other species of bacteria, and which involve whole lobes. 



THE RESPIRATORY SYSTEM. 439 

blood cells, and epithelial cells (see Fig. 208). The epithelium re- 
maining on the walls of the air spaces is swollen; there are large 
numbers of white blood cells in the capillaries. The larger bronchi 
are congested, dry, or coated with mucus ; the small bronchi contain 
the same inflammatory products as do the air spaces. The pulmo- 
nary pleura, as a rule, is not coated with fibrin. This is called the 
stage of "congestion." The stage of congestion regularly only lasts 
a few hours, but it may be protracted for several days. 

When the exudation of the inflammatory products has reached 








4 



■Fig. 208.— Acute Lobar Pneumonia— Red and Gray Hepatization, x 850 and reduced. 
Showing the pneumococci of Frankel in the exudation, stained violet. 

its full development the presence of these products within the air 
spaces and bronchi causes the lung to be solid, and at this time the 
lung is said to be in the condition of "red hepatization." The lung 
is now consolidated, red, its cut section looks granular, the granules 
corresponding to the plugs of inflammatory matter within the air 
spaces. For some time after death the inflammatory products re- 
main solid and -the cut section of the lung dry ; but later, with the 
commencement of post-mortem changes, these products soften and 



440 



THE RESPIRATORY SYSTEM. 



the cut section is covered with a grumous fluid. The air vesicles, th 
air passages, the small bronchi, and sometimes the large bronchi, ar 
filled and distended with fibrin, pus cells, red blood cells, and epithe 
lium, and may contain large numbers of bacteria (Fig. 208). I 
spite of the pressure on the walls of the air spaces the blood vessel 
in their walls remain pervious. The pulmonary pleura is coate 
with fibrin and the interstitial connective tissue of the lung is infi 
trated with fibrin. The hepatized lobe is increased in size, some 
times so much so as to compress the rest of the lung. About one 
fourth of the fatal cases die in the stage of red hepatization at an 
time from twenty-four hours to eleven days after the initial chill. 




Fig. 209.— Acute Lobar Pneumonia with the Production of Organized Tissue in the A 
Spaces, x 130 and reduced. 

The section shows a number of air vesicles containing organized tissue. 



After the air spaces have become completely filled with the exi 
dation, if the patient continues to live, there follows a period durin 
which the exudate becomes first decolorized and then degeneratec 
This is the period of "gray hepatization." The lung remains solk 
its color changes, first to a mottled red and gray, then to a unifon 
gray. The coloring matter is discharged from the red blood eel 
and the exudate begins to degenerate and soften. The lung is four 
passing from red to gray hepatization at any time between tr 



THE RESPIRATORY SYSTEM. 



Ul 



second and the eighteenth day of the disease. It is found com- 
pletely gray at any time from the fourth to the twenty-fifth day. 
About one-half of the cases die in the condition of mottled red and 
gray hepatization ; about one-fourth in the condition of gray hepa- 
tization. 

If the patient recovers the exudate undergoes still further de- 
generation and softening and is removed by the lymphatics. This 
is the stage of " resolution." It should commence immediately after 



r 





^ 



^ 



^ 



Fig. 210.— Organized Tissue in an Air Vesicle, x 850 and reduced. 



defervescence and be completed within a few days. But it may not 
begin until a number of days after defervescence, or it may be un- 
usually protracted. 

The pneumococcus of Frankel (often also called the Diplococcus 
pneumoniae of Frankel) is the bacterium most often present in the 
lungs in acute lobar pneumonia, and the form which there is much 
reason to believe, in the large proportion of cases, to be the cause of 
the disease. The germ is described on page 201. 

There is a form of lobar pneumonia in which the inflammation is 
not simply an exudative one, but there is also a growth of new con- 
35 



442 



THE RESPIRATORY SYSTEM. 



nective tissue in the walls of the air spaces and in their cavitk 
(Fig. 209). 

This condition has been usually described as a chronic inflan 
mation following an ordinary lobar pneumonia. It seems really t 
be from the outset a special form of pneumonia. For we find, i 
patients who have not been sick for more than a few days, that th 
pneumonia already has its characteristic form. Still further, eve 
in its earlier stages the clinical history is somewhat different f roi 
that of an ordinary lobar pneumonia. 




Fig. ^11.— Air Vesicles containing Organized Tissue in Lobar Pneumonia, x 350 and reduce^ 
The blood vessels are injected. 



If the patient dies within three weeks of the commencement c 
the pneumonia we find one or more lobes consolidated but not muc 
enlarged. The hepatization is smooth and dense. The walls of th 
air spaces are thickened and coated with an increased number c 
epithelial cells. Some of the air spaces contain only fibrin and pus 
"but in others there is new connective tissue, basement substance an 
cells (Fig. 210). In this new tissue there may be new blood vessels 
which can be artificially injected from the vessels of the lung (Fig 
211). 



THE RESPIRATORY SYSTEM. 



443 



If the patient lives for several months we find the lung very 
dense and smooth. The growth of new connective tissue is more ex- 
tensive, the air spaces are completely filled, their walls are much 
thickened, and in some places the lung tissue is completely changed 
into smooth connective tissue. 




Fig. 212.— Broncho-Pneumonia from a Child. 
The walls of the bronchi thickened with zones of peribronchitic pneumonia. 



II. Broncho-pneumonia (Capillary Bronchitis, Lobular Pneu- 
monia, Catarrhal Pneumonia). 

This is the ordinary pneumonia of young children ; it is frequent 
also in young persons, but not as common in adults. 

In children it seems to be usually due to causes similar to those 
which produce lobar pneumonia in adults — that is, to micro-organ- 
isms, especially the pyogenic cocci, and sometimes to the inhalation 
or inspiration of inorganic irritating substances. 

In adults the disease may present itself to us in a variety of ways. 

1. The patients have an ordinary attack of catarrhal bronchitis 
lasting for several days. Instead of getting well promptly, how- 



444 THE RESPIRATORY SYSTEM. 

ever, the patients continue to cough and to feel sick, and on examin- 
ing the chest we found a circumscribed area where there is dul 
ness on percussion and loud, high-pitched voice. This consolidation 
of the lung does not, however, last very long, and the patients 
make a good recovery. 

2. The patients are suddenly attacked with a very severe anc 
general broncho-pneumonia. There are chills, a rapid rise of tern 
perature, headache, pains in the back and chest, vomiting, grea- 
prostration, a rapid pulse which soon becomes feeble, very bac 
breathing— rapid, labored, and insufficient — venous congestion of the 
skin and of the viscera, cough, at first dry, then with profuse mucus 
and blood-stained sputa, sleeplessness, restlessness, and delirium 
and albumin in the urine. There are coarse subcrepitant and crepi 
tant rales over both lungs, sibilant and sonorous breathing ; the per 
cussion note is normal, or exaggerated, or dull. The disease lasts 
for from seven to fourteen days, and is very apt to prove fatal. 

3. There is a form of broncho-pneumonia in adults which re 
sembles lobar pneumonia. There is a general catarrhal bronchitis 
with broncho-pneumonia and consolidation of one or more lobes, 
The symptoms and physical signs are like those of lobar pneumonia, 
but with some difference. The invasion of the disease is not as sud- 
den, the pulse is more rapid, the cerebral symptoms are more con- 
stant, the expectoration is like that of bronchitis, the physical signs 
are more slowly developed, the duration of the disease is rathei 
longer and resolution is slower. 

4. There is a form of broncho-pneumonia which resembles acute 
phthisis. The patients have a cough with expectoration, at flrsl 
mucous, afterward muco-purulent. There is a moderate fever, witfc 
evening exacerbations and sweating at night. The patients steadily 
lose flesh and strength. The physical signs are those of bronchitis 
and of consolidation of parts of the lung. The disease is protracted, 
continuing as long as ten weeks, and is apt to prove fatal. 

With substantive emphysema there may be developed a subacute 
or chronic broncho-pneumonia. 

The essential or constant lesion of broncho-pneumonia is an in 
flammation of the walls (not the mucous membrane) of the bronch 
and of the air spaces immediately surrounding the inflamed bronchi, 
The walls of the bronchi are thickened and infiltrated by a growtr 
of new cells. The walls of the air spaces are thickened, their cavi- 
ties are filled with fibrin, pas, and epithelium or with new connec- 
tive tissue. The inflammation, involves the medium-sized and 
smaller bronchi of both lungs, but. is not everywhere equally severe 
in some parts of the lungs the lesions are much more marked thar 
in others. In some of the cases there are no other changes excepl 
some general congestion of the lungs. In other cases there may be 



THE RESPIRATORY SYSTEM. 



445 



added a catarrhal inflammation of the mucous membrane of the 
bronchi, diffuse consolidation of parts of the lung, pleurisy, dilata- 
tion of the inflamed bronchi, areas of atelectasis, simple or tubercu- 
lar inflammation of the bronchial glands. 

The trachea and the larger bronchi are congested and coated with 
mucus. The smaller bronchi contain pus, their walls are thickened 
and infiltrated with cells, and they may be dilated. Around many 











w* 



■ 



I ^ 



- 

^J 



Fig. 213.— Bboncho-pneumonia in a Child, x 750 and reduced. 
Air vesicles in diffuse hepatization. 

of the small bronchi are narrow zones of congestion or hepatization 
The rest of the lungs is congested and cedematous. 

Or the zones of peribronchitic pneumonia are larger, so that a sec- 
tion of the lung is mottled with little whitish nodules, each nodule 
corresponding to a cut bronchus surrounded by its zone of pneumonia. 

Or between these zones of peribronchitic pneumonia are areas of 
diffuse hepatization which render portions of the lung completely 
solid (Fig. 213): 

Or there may be areas of atelectasis corresponding to occluded 
bronchi. 



446 



THE RESPIRATORY SYSTEM. 



There is often a thin layer of fibrin on the pulmonary pleura 
The bronchial glands are the seat of simple or tubercular inflamma 
tion. 

The dilatation of the bronchi is not constant. When present it i 
of the cylindrical character and involves the medium-sized broncl 
for a considerable part of their length. Such dilated bronchi ai 
each of them surrounded by a narrow zone of pneumonia ; the intei 
vening lung tissue may be still aerated or hepatized. 

In these peribronchitic zones of pneumonia the thickening an 
cellular infiltration which exist in the walls of the bronchi exten 



Ji 









W£ 




Fia. 214.— Broncho-pneumonia in an Adult, x 850 and reduced. 
An air vesicle containing organized tissue in a zone of peribronchitic pneumonia. 

also to the walls of the air spaces. These walls are thickened an< 
infiltrated with cells, while the cavities of the vesicles are filled wit] 
pus and epithelium or with tissue resembling granulation tissue (Fig 
214). In the diffuse hepatization the air vesicles are filled witl 
epithelium, pus, and fibrin in varying proportion and quantity ; th 
walls of the air spaces remain unchanged. 

The portions of lung which are not hepatized are congested anc 
oedematous. The cavities of the vesicles are diminished by the en 
larged capillaries, the epithelium is swollen, and in many vesicles i 
few pus or epithelial cells are to be found. 



THE RESPIRATORY SYSTEM. 



447 



Such a broncho-pneumonia differs from the ordinary lobar pneu- 
monia very decidedly. The inflammatory process is not a superfi- 
cial one, resulting only in filling the bronchi and air spaces with in- 
flammatory products, but it affects also the tissue of the lung, infil- 
trating the walls of the bronchi and of the air spaces. 

This interstitial character of the inflammation seems to be the 
reason why the disease is often protracted and sometimes succeeded 
by a chronic inflammation. TlnV chronic condition we will call 
" Persistent Broncho-pneumonia." 




Fig. 215.— Persistent Broncho-pneumonia. 

The original acute broncho-pneumonia is succeeded by a chronic 
inflammation involving especially the interstitial tissue. 

This inflammation may involve only some of the smaller bronchi 
and small zones of vesicles around them, and then a section of the 
lung will seem to be studded with fibrous nodules (Fig. 215). Or all 
the bronchi of some part of the lung will be inflamed, the peribron- 
chitic zones of pneumonia will become continuous, and so part of a 
lobe or an entire lobe become converted into a dense mass of con- 
nective tissue. The air vesicles are obliterated by the new connec- 
tive tissue, the- interlobular septa and the pulmonary pleura are 
thickened (Fig. 216), and the inflamed bronchi may be dilated. The 
blood vessels, however, are, for the most part, not obliterated, so 



448 



THE RESPIRATORY SYSTEM. 



that the lung does not become necrotic or degenerated, althoug 
occasionally areas of cheesy degeneration exist. 

III. Secondary and Complicating Pneumonia. 

Inflammation of the lungs occurs frequently as a complicatir 
condition with lesions of the brain and spinal cord, with pysemi 
with the continued fevers, after injuries and surgical operations, ar 
in patients who are confined to bed for a long time from any cause. 

The pneumonia developed in these cases may f ollow one of tv 
different types. 




%, 




Fig. 216.— Persistent Broncho-pneumonia. 




1. Part of the lung, usually the posterior portion, is congeste 
leathery, only partly aerated, and mottled by irregular patches < 
red or gray hepatization which have no relation to the bronchi. ] 
the hepatized portions of the lung the air spaces are filled with pi 
and fibrin. 

2. The inflammation has the characters of a broncho-pneumonu 
The small bronchi are filled with pus, their epithelium is alterec 
their walls are infiltrated with pus, and around each bronchus is 
zone of air vesicles filled with pus and fibrin. The lung is mottle 
with little whitish nodules, corresponding to the bronchi and tt 



THE RESPIRATORY SYSTEM. 



449 



peribronchitic zones, and between these there may be a diffuse hepa- 
tization. 

In children suffering from diphtheria, with pseudo-membranes 
containing pathogenic bacteria in the fauces and upper air passages, 
a secondary pneumonia may apparently occur as the result of the 
entrance into the lung spaces of the germs from above (Fig. 217). 1 
Although the pyogenic bacteria are the most frequent inciters of 
secondary and complicating pneumonia, other forms of germs are 
capable of inducing it. 




Fig. 21?.— Bronchopneumonia in a Child, complicating Diphtheria. 

Air vesicle showing inflammatory products and large numbers of bacteria (streptococci) 
stained with methyl violet. 

IV. The Pneumonia of Heart Disease. 

Lesions of the aortic and mitral valves, and dilatation of the left 
ventricle, often produce a diffuse, chronic inflammation of both lungs 
of a peculiar character. This condition is often called pigment in- 
duration, or brown induration, but it is really a chronic pneumonia. 

The lungs are diminished in size and of a peculiar yellow-pink 
color, mottled with spots of black or brown pigment. They are not 
congested, but are of a dry, leathery consistence ; or portions of them 

1 Consult Prudden and Nbrthrup, " Studies on the Etiology of Pneumonia com- 
plicating Diphtheria in Children," American Journal of Medical Sciences, June, 1889. 
36 



450 THE RESPIRATORY SYSTEM. 

may be in the condition of a smooth red hepatization. The appe; 
ance of these lungs may be modified by the presence of hsemorrha^ 
infarctions, by the pre-existence of emphysema, or by oedema. 

Minute examination of these lungs shows four separate patholo; 
cal conditions. 

1. A change in the capillaries in the walls of the air spac 
These capillaries are dilated and tortuous, so that they project ii 
the cavities of the vesicles (Fig. 218). The degree of the dilatati 
varies in the different lungs ; in some it is very marked, in othe 
but light. 

2. A thickening of the walls of the air spaces, due partly to i 

& 










iff • -< ti* " -'^ M 

Fig. 218.— Lung of Heart Disease. 
Showing dilated capillaries of the walls of the air vesicles and the presence of hasmatogen 
Digment in the exfoliated epithelial cells of the air vesicles. 

dilatation of the capillaries, partly to a growth of smooth muse 
and partly to a growth of connective tissue. The degree of t 
thickening varies very much in different cases. 

3. A formation of black or brown pigment in the shape of grs 
ules and small masses. This is deposited in the walls of the vesicL 
in the interstitial connective tissue, and in the new cells within t 
vesicles (Fig. 218). 

4. A formation of cells within the air spaces. The walls of t 
vesicles are coated with a layer of flat, nucleated cells. Similar eel 
or swollen and granular cells, are present in the cavities of t 



THE RESPIRATORY SYSTEM. 451 

vesicles (Fig. 218). If these cells are numerous the cavities of the 
vesicles are filled, and there results a smooth red hepatization. 

V. Interstitial Pneumonia. 

This name is given to a chronic productive inflammation, which 
involves the connective-tissue framework of the lung and the walls of 
the air spaces, and results in the formation of new connective tissue 
and the obliteration of the air spaces (Fig. 219). 

Such an interstitial pneumonia may follow acute lobar pneumonia 



v^w 










Fig. 219.— Interstitial Pnettmoxia, x 90 and reduced. 
From a case of chronic phthisis. 

with the production of new connective tissue; broncho-pneumonia; 
chronic pleurisy; chronic bronchitis; or be caused by the inhalation 
of the dust of coal or of stone. 

The condition of the lung varies with the cause of the interstitial 
pneumonia. 

If it follows acute lobar pneumonia with the production of new 
connective tissue, one lobe, or the whole of one lung, is covered with 
pleuritic adhesions. The lobe or the lung is small, smooth on sec- 
tion and dense. The air spaces and small bronchi are obliterated by 
the new connective tissue. 

If it follows broncho-pneumonia, one or more lobes are studded 



452 THE RESPIRATORY SYSTEM. 

with fibrous nodules, which correspond to the inflamed bronchi ; c 
the whole of a lobe is converted into dense fibrous tissue. The pleur 
is thickened, the bronchi are inflamed and often dilated. 

If it follows thickening of the pleura, bands of connective tissu 
extend from the pleura into the lung, the bronchi are inflamed an 
often dilated. 

If it follows chronic bronchitis, there are fibrous nodules aroun 
the bronchi, with more or less diffuse connective tissue. 

If it is due to the inhalation of coal or dust, we find in both lung 
fibrous peribronchitic nodules and diffuse connective tissue. 

When only one lung is involved the other is apt to be emphysem 
atous. 

Suppurative interstitial pneumonia is sometimes produced in case 
of septicaemia. The pulmonary pleura is coated with fibrin, th 
bronchi contain pus, portions of the lung are hepatized, and the in 
terlobular septa are infiltrated with pus. 

VI. Tuberculous Pneumonia. 

We employ the name of " tuberculous pneumonia" to designate tb 
inflammations of the lungs which are caused by the introduction o 
tubercle bacilli into these organs. Such tuberculous inflammation 
of the lungs may be confined to them, or they may be aceompanie< 
by tuberculous inflammations of other parts of the body. 

For the development of a tuberculous inflammation there seem t< 
be necessary the irritation of the tissues caused by the tubercle bacill 
and a predisposition on the part of the individual. 

The development of such an inflammation in any part of the bod] 
is also favored by the conditions which favor or the causes whic] 
induce other phases of inflammation. 

The tubercle bacilli are capable of setting up different anatomica 
forms of inflammation, either separately or together. They may giv< 
rise to exudation from the blood vessels, to the production of nev 
tissue, or to necrosis (see page 218). 

The introduction of tubercle bacilli into the lungs, therefore, ma] 
produce: an exudative inflammation with fibrin and pus cells in tin 
air spaces ; a productive inflammation with the growth of epithelia 
cells, or of round-celled tissue, or of a tissue composed of basemen 
substance, large and small cells, and giant cells, called tubercL 
tissue (see page 21 7) ; or there may be added necrosis of the nev 
tissue and of portions of the lung. 

The character of the inflammation in each case seems to be gov 
erned by the number of bacilli which are introduced into the lungs 
and the way in which they are introduced, as well as by the suscepti 






THE RESPIRATORY SYSTEM. 453 

bility of the individual. If a large number of tubercle bacilli are 
inhaled through the bronchi, both productive and exudative inflam- 
mations ma}' be set up in a considerable portion of the lungs. If, on 
the other hand, but a small number of bacilli are inhaled, or if these 
find their way into the lungs through the blood vessels or lymphatics, 
then there are small foci of prod active inflammation with but little 
exudation. 

There are two ordinary ways in which the lungs are infected : 
(a) The bacilli which float in the air are inhaled and irritate 
the small bronchi and the air spaces; (b) the bacilli contained in a 
focus of tuberculous inflammation in some other part of the body are 
carried by the blood vessels to the lungs, become lodged there and set 
up small areas of inflammation. 

The changes in the lungs may also be modified by an infection 
with other pathogenic micro-organisms. 

As the gross appearance of the lungs varies with the character, 
extent, and development of the different phases of inflammation excited 
by the tubercle bacilli, a number of arbitrary names have been given, 
which may still be conveniently used. We describe, therefore, 
Acute Miliary Tuberculosis; Subacute Miliary Tuberculosis; 
Chronic Miliary Tuberculosis; Acute Phthisis and Chronic 
Phthisis. 

Acute Miliary Tuberculosis. — The acute development of miliary 
tubercles in the lungs is usually only part of general tuberculosis, 
although the lesion may be most extensive in the lungs. 

Both lungs are apt to be involved, but the distribution, number, 
size, and character of the miliary tubercles differ in different cases. 

The larger bronchi are the seat of catarrhal inflammation ; the 
lung tissue is congested; the air spaces contain epithelium, pus, and 
fibrin in small quantity. 

The tubercles are found in the parenchyma of the lung, in the 
connective tissue forming the septa, along and in the walls of the 
bronchi and blood vessels, and in the pulmonary pleura. 

They are scattered singly through the lungs, or aggregated in 
groups. They may be separated by considerable interspaces, or so 
close together that the lung is rendered nearly solid. Some are so 
small and transparent that they can hardly be seen with the naked 
eye; others are larger and more opaque. In children's lungs large 
masses are found of the same structure as miliary tubercles. 

In many cases it seems evident that the lungs are infected through 
the blood vessels, or perhaps through the lymphatics, for the general 
tuberculous infection is secondary to a localized tuberculosis of some 
other part of the body. But in other cases no such localized primary 
focus can be found, so that infection by inhalation is possible. The 



454 



THE RESPIRATORY SYSTEM. 



whole picture of acute tuberculosis is such, however, as to give tJ 
impression that the infection usually takes place through the blot 
vessels and lymphatics. 

The anatomical forms of miliary tubercles are as follows : 

1. Miliary tubercles composed of a group of air vesicles contai: 

ing amorphous granular matter, with a few shrunken cells and i 

external zone of pus cells. The walls of the air spaces may be st: 

visible, and may be infiltrated with exudate, or they may be necrot 




Fig. 220.— Miliary Tubercle in Lung of Child. 
Showing the- Bacillus tuberculosis— stained with fuchsin— in the contents of the air vesicles a 
in their thickened walls. (The size of the bacilli relative to other elements is slightly exaggerate< 



and lost in the mass of granules. The only changes are exudatic 
and necrosis (Fig. 220). 

In adults such tubercles are usually small, but in children the 
may reach a large size. 

2. Miliary tubercles formed by the infiltration of the wall of 
bronchiole or air passage with tubercle tissue or granulation tissu 
This infiltration is apt to involve only one side of the bronchiole < 
air passage (Fig. 221). It may be confined to this or it may extern 
to the walls of the adjacent vesicles. These vesicles may remai 



THE RESPIRATORY SYSTEM. 



455 



empty, they may be dilated, or they may be filled with tubercle tissue 
or with epithelium, fibrin, and pus. 

In these tubercles we see productive inflammation by itself in 
some cases, combined with exudation in others. The inflammation 
seems to begin in the walls of the small bronchioles and to extend 
from them to the adjacent air spaces. 




Fig. 221— A Peribronchitic Miliary Tubercle. 



In all miliary tubercles there is often cheesy degeneration of the 
central portions. Although all miliary tubercles are caused by the 
presence of tubercle bacilli, it may be quite difficult to demonstrate 
the bacilli in each. These tubercles are formed by a combination of 
productive and exudative inflammation which involves groups of air 
spaces. 

3. Miliary tubercles composed of a group of air spaces of which 
the walls are infiltrated and the cavities filled (Fig. 222) with granu- 



456 



THE RESPIRATORY SYSTEM. 



lation tissue or tubercle tissue ; as the infiltration progresses the bloo 
vessels are obliterated (Fig. 223). Such an infiltration may involv 
symmetrically the whole of the wall of an air space, or only a poi 
tion of the wall. The cavities of the air spaces are filled with tubei 
cle tissue, or with epithelium, fibrin, and pus. 

In some of these tubercles the tubercle tissue, both in the walls c 
the air spaces and in their cavities, is well developed (Fig. 224) ; the 
they look like little tumors replacing the lung tissue. In others th 
outlines of the walls of the vesicles are preserved, granulation tissu 
predominates, the cavities of the vesicles contain pus, epithelium 
fibrin, and less tubercle tissue (Fig. 225); then the tubercle look, lik 
little areas of a composite hepatization. 




fWWM #V0" 




Fig. 222.— An Aggregation of Miliary Tubercles, x 90 and reduced. 



~#1C mm 



Subacute Miliary Tuberculosis. — The disease usually involve 
only the apex of one lung, or one lobe, or portions of both lungs 
The inflammation may continue for weeks or months, then stop am 
the patient recover. Or the patient may have a number of attacks 
from each one of which he recovers. Or the disease may con 
tinue, extend, and cause death within a few months. Or it may b 
succeeded by chronic miliary tuberculosis. 

The miliary tubercles are small. Most of them are formed withii 
the air spaces or around the bronchioles. They are composed princi 
pally of tubercle tissue or of round -celled tissue. In the portion o 
lung where the tuberculous inflammation is going on there may als< 
be localized catarrhal bronchitis and pleurisy. 



THE RESPIRATORY SYSTEM. 



457 



It seems evident that the infection is produced by a small number 
of bacilli, and that the principal effect of their presence is a produc- 
tive inflammation of the walls of the air spaces and of the small 
bronchi. It is much to be regretted that we are still uncertain as to 
the method of infection in these cases. There is no demonstration 
as to whether the bacilli are usually introduced through the bronchi 
or the blood vessels. 




Fig. 223 — A Miliary Tubercle, x 300 and reduced 
Involving only two air vesicles, of which the walls are infiltrated and the cavities filled with 
tubercle tissue. The blood vessels of the air vesicles are injected. 



Chronic Miliary Tuberculosis. — The morbid process is apt to 
begin at the apex of one lung and then slowly extend, either pro- 
gressively or in attacks, until a large part of the lungs is involved. 

The whole course of the disease is such as to give the impression 
of an infection through the blood vessels and lymphatics and not by 
inhalation. The inflammation excited is of the productive form 
running a slow course. 
37 



458 



THE RESPIRATORY SYSTEM. 



In the simplest form of the disease the only change in the lungs 
the formation of miliary tubercles. These tubercles are harder ai 
denser than those found with general tuberculosis or with subacu 
pulmonary tuberculosis. They are composed of tubercle tissue, 
round-celled tissue, or connective tissue, or are in the condition 
cheesy degeneration. 

Usually, however, in addition to the miliary tubercles there a 
other changes in the lungs. These additional lesions begin in tl 










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Fig. 224.— A Miliary Tubercle, x 330 and reduced. 
Formed of several air vesicles filled with tubercle tissue and surrounded by a zone of tiss 
resembling granulation tissue. 

same part of the lung where the tubercles are formed, and accompan 
the development of the tubercles in fresh parts of the lungs. 

There may be a localized catarrhal bronchitis. 

There may be an inflammation of the walls of the bronchi, wit 
partial destruction of these walls and the formation of cylindrical ( 
sacculated bronchiectasis. The walls of the cavities thus forme 
may be converted into connective tissue, or they may remain suppi 
rating and necrotic. 



THE RESPIRATORY SYSTEM. 



459 



There may be an interstitial pneumonia with the production of 
new connective tissue, the obliteration of the air spaces, and the con- 
solidation of portions of the lungs. 

There may be dilatation of the air spaces of the portions of the 
lungs which are not consolidated. 

There may be thickening of the pulmonary and costal pleura, with 
connective-tissue adhesions. 

While the morbid process begins as a localized tuberculous inflam- 
mation of the lungs, and often retains throughout this local charac- 
ter, yet it may also happen that from this local lesion other parts of 
the body may be infected. Tuberculous laryngitis, and tuberculous 



jSs5^V/v.t '/^ ; 






ill II 

















Fig. 225.— A Miltary Tubercle, X 300 and reduced. 
Formed of a number of air vesicles, some containing tubercle tissue, otbers pus and epithelium. 



inflammation of the solitary and agminated lymph nodules of the 
small intestine, often complicate the pulmonary lesion, and some- 
times even acute general tuberculosis is produced. 

Acute Pulmonary Phthisis. — This name is used to designate the 
tuberculous inflammation of the lungs in which exudative inflamma- 
tion preponderates, but is associated with productive inflammation. 
It seems evident that this feature of the inflammation is due to the 
large number of bacilli introduced by inhalation through the bronchi, 
or which rapidly grow in the long, and to the frequent association 
of an infection with other bacteria, especially streptococci. 

The changes produced in the lungs by the introduction into the 
bronchi of tubercle bacilli can be well studied in animals. One of us 



460 



THE RESPIRATORY SYSTEM 



(Prudden) 1 by the injection of tubercle bacilli alone and associati 
with streptococci into the tracheae of rabbits has been able to repr 
duce very closely the lesions of acute phthisis. 





Fig. 226. Fig. 227. 

Fig. 226.— Experimental Tuberculous Inflammation (Miliary) in the Lung op a Rabbit 
The rabbit's lung shows miliary foci of tuberculous inflammation, twenty-two days after 
injection through the trachea of a small quantity of broth culture of the tubercle bacillus. 

Fig. 227.— Experimental Tuberculous Inflammation in the Lung of a Rabbit. 
Large areas of solidification in the lung twenty-eight days after the injection through 
trachea of a considerable quantity of a pure culture of the tubercle bacillus. The lesions res< 
ble those of acute phthisis in man. 

If a small quantity of a pure culture of the tubercle bacillus 
very minute flocculi is mixed with a considerable quantity of s: 

1 New York Medical Journal, July 7th, 1894. 






THE RESPIRATORY SYSTEM. 461 

solution and introduced into the lungs through the trachea a number 
of small areas of consolidation are produced which have the gross 
appearance of miliary tubercles (Fig. 226). These small areas of 
consolidation are composed of epithelial cells and leucocytes. After 
the development of these cell masses, which may occur within a few 
hours, they may remain with little apparent change, or become more 
or less infiltrated with leucocytes, or become cheesy, or be surrounded 
by a dense zone of small spheroidal cells. 

When larger quantities of the tubercle bacillus are introduced 
into the lungs through the trachea large areas of consolidation are 
formed (Fig. 227), which may involve whole lobes or whole lungs. 
The first effect upon the lungs is the collection about the bacilli, in 
the air spaces where they have lodged, of dense masses of leucocytes. 
These cell collections immediately about the germs form the centres 
of the inflammatory foci which develop later. They correspond in 
shape to the shapes of the small bronchi and the connecting airspaces 
in which the bacilli have lodged. The walls of these cell-filled spaces 
may soon become necrotic, even within twenty-four hours. The 
blood vessels about these intra-alveolar masses of small cells and 
tubercle bacilli are intensely congested, and within forty-eight hours 
a considerable proliferation of alveolar epithelium has occurred in the 
zone of air spaces surrounding the primary foci. Giant cells may 
form in the air spaces, apparently by the fusion of the new-formed 
epithelial cells. The changes of a productive inflammation may 
begin in the walls of the air spaces about the primary small-celled 
foci as early as the third day. The smaller bronchi belonging to the 
involved air spaces may also be densely packed with small spheroidal 
cells. Within the first three days, if the quantity of injected 
tubercle bacilli be large, the air spaces about the involved areas may 
be the seat of an exudative inflammation, so that they are closely filled 
with fibrin and leucocytes as well as' with epithelium. Almost as 
soon as they have collected a large, part of the leucocytes about the 
tubercle bacilli may die, so that within three days after the intro- 
duction of the bacilli these cell masses are converted into a granular 
mass — coagulation necrosis — in which only the nuclei can be distin- 
guished. The tubercle bacilli are confined to these central cell masses, 
so that both the epithelial cell proliferation and the exudative inflam- 
mation appear to result from some soluble product of the tubercle 
bacillus which may be diffused. 

As time passes the naked-eye distinction is maintained between 
a larger or smaller irregular-shaped central white area of consolida- 
tion, the seat of lodgment of the bacilli, and a surrounding translu- 
cent zone of consolidated lung which contains few bacilli. The cen- 
tral mass of necrotic cells and lung tissue gradually undergoes 



^^ 



462 



THE RESPIRATORY SYSTEM. 



coagulation necrosis and increases in size by encroachment on the 
surrounding zone of consolidation. The translucent border zone of 
consolidation grows wider, the air spaces in it are rilled with epithe- 
lium, fibrin, and leucocytes. There is a growth of new tissue in the 
walls of the air spaces. Giant cells are often abundant in this zone. 
The changes thus far indicated are such as may occur within the 
first two weeks after the injection of the bacilli. From this time on 




Fig, 228.— Experimental Tuberculous Inflammation in the Lung op a Rabbit, with the 

Formation op Cavities. 
The lung was injected with a considerable quantity of tubercle-bacillus culture through the 
trachea, followed after twenty-eight days by the injection of the broth culture of the strepto- 
coccus pyogenes. Animal killed seven days after the streptococcus injection. The specimen 
shows large areas of consolidation with cavities. The lesions resemble those of acute phthisis 
with cavities in man. 



up to the seventh week the changes are quantitative rather than 
qualitative. The central necrotic mass may become fully cheesy, 
and may grow slowly larger by encroachment upon the surrounding 
zone of epithelial cell proliferation and productive and exudative in- 
flammation. The areas of consolidation may coalesce so as to render 
whole lobes or lungs solid, so that to the naked eye the cut surface 



THE RESPIRATORY SYSTEM. 



463 



presents an irregular mottling with large or small white masses and 
more translucent intervening areas. The intima of the large blood 
vessels near the involved areas may be thickened and smaller trunks 
may be obliterated. 

In the presence of the tubercle bacillus alone the cheesy areas but 
rarely soften and break down so as to form cavities. If, however, 
after the tuberculous inflammation of the lung has been produced and 
allowed to continue for a number of days, a culture of Streptococcus 




Fig. 229.— Tuberculous Broncho-pneumonia. 
The walls of the bronchi are thickened and surrounded by zones of pneumonia. 



pyogenes be introduced into the trachea in a rabbit, within twenty- 
four hours the cheesy areas begin to soften. The softening may be- 
gin at the centre of a cheesy area, or may surround a central portion 
of the necrotic mass. The softening is soon followed by absorption, 
and so cavities are formed of varying size's and shapes (Fig. 228) . 

It will thus -be seen that in the rabbit a concurrent infection with 
the tubercle bacillus and the streptococcus has an important bearing 




464 



THE RESPIRATORY SYSTEM. 



upon the breaking clown of lung tissue which leads to the formation 
of cavities. While it would not be wise to assume from these ex- 
periments on the rabbit that a similar condition exists in man, it 
will be seen presently (page 467) that in fact a similar concurrent 
infection in man in acute phthisis actually does often exist. 

The tuberculous inflammation of the lungs in human beings pro- 





Fig. 230. 



-An Area of Coagulation Necrosis surrounded by a Zone of Pneumonia, 
X 40 and reduced. 



duced by the inhalation of a large number of tubercle bacilli pre- 
sents five varieties which have well-marked anatomical and clinical 
characteristics. 

I. In one or more lobes there are miliary tubercles in considerable 
numbers, and a diffuse hepatization. The miliary tubercles have the 
structure already described under the head of acute tuberculosis. 
The diffuse hepatization is like that of lobar pneumonia — the air 
spaces are filled with fibrin, pus, and epithelium. 



THE RESPIRATORY SYSTEM. 



465 



This form of acute phthisis is not of common occurrence. If an 
entire lung is con so] i dated the patients usually die within a short 
time. If only one lobe is involved, it is possible for them to recover, 
for the fibrin, pus, and epithelium to be absorbed, and only the miliary 
tubercles left as a permanent change. 

II. There is a general catarrhal bronchitis and a tuberculous in- 
flammation of the walls of some of the bronchi and of small zones of 
air spaces immediately surrounding them, but there is no diffuse con- 
solidation. The inflammation of the walls of the bronchi is produc- 
tive with the formation of tubercle tissue and round-celled tissue. 









Fig. 231.— Tuberculous Inflammation op the Lung with Cheesy Degeneration about the 
Bronchi in a single Lobule of the Lung — Acute Phthisis. 

That of the surrounding zone of air spaces is partly productive, partly 
exudative. Some of the air spaces are filled with epithelium or with 
fibrin and pus, some with tubercle tissue. 

In these patients the only physical signs are those of the general 
bronchitis. If the lesion is not too extensive recovery is possible. 

III. There is a catarrhal bronchitis, a tubercular inflammation of 
the walls of the bronchi and of the air spaces surrounding them, and 
a diffuse consolidation of rather complex character. 

One or more lobes are competely consolidated, while in other 
parts of the lung there are little whitish nodules, but no general con- 
38 



466 THE RESPIRATORY SYSTEM. 

solidation. The consolidated portion of lung is not of uniform 
appearance. It is evidently made up of white or yellow areas of 
different sizes and shapes, surrounded by zones of red or grayish 
hepatization. The blood vessels of the white and yellow areas are 
occluded and cannot be injected, the vessels of the surrounding zones 
of hepatization are pervious. The white and yellow nodules are 
formed in three different ways. 

1. One or more air passages with the air vesicles belonging to 
them have their cavities filled with fibrin, pus, epithelium, and 
tubercle tissue, while their walls are more or less infiltrated with 
tubercle tissue. The tubercle bacilli find their way into these air 
passages and excite an inflammation which is principally produc- 
tive. 

2. There is an inflammation of the walls of the small bronchi and 
of the air spaces around them so that on section these bronchi and 
associated air spaces look like nodules. These little bronchi are 
inflamed in three ways: (a) The bronchus contains pus and. epithe- 
lium, its wall is infiltrated with round cells, the surrounding air 
spaces are filled with epithelium, pus, and fibrin. (6) The wall cf 
the bronchus is infiltrated with tubercle tissue and the surrounding 
air spaces contain tubercle tissue, (c) There is no change in the wall 
of the bronchus, but the surrounding air spaces contain tubercle tissue. 
The tubercle bacilli lodge in the small bronchi and set up exudative 
or productive inflammation in their walls and in the air spaces which 
surround them. 

3. There are small or larger areas of the lung in the condition of 
coagulation necrosis or of cheesy degeneration. These areas are sur- 
rounded by zones of exudative or of productive inflammation. They 
correspond exactly to the changes produced in the lungs of rabbits by 
the injection of tubercle bacilli into the trachea. It is from the 
rabbit's lungs that we can learn the early stages in the formation of 
these areas of coagulation necrosis. The tubercle bacilli lodge in 
groups of air spaces and set up in them an exudative inflammation. 
These air spaces are quickly filled with pus and epithelium, and the 
blood vessels in their walls become obliterated. Then follow degen- 
eration, coagulation necrosis, and cheesy degeneration. At the same 
time these necrotic areas seem to act as irritants and around them are 
set up zones of exudative or productive inflammation. In the diffuse 
hepatization between the nodules the blood vessels remain pervious 
and can be readily injected. The air spaces are more or less com- 
pletely filled with inflammatory products. The inflammatory prod- 
ucts are: pus cells, fibrin, large epithelial cells, minute shining 
granules, and a peculiar transparent substance. Some air spaces are 
entirely filled with granules, others with fibrin, others with epithelial 



THE RESPIRATORY SYSTEM. 



167 



cells, and still others with pus cells, while in still other air spaces 
these products are combined in different proportions. 

IV. In a certain number of the cases of acute phthisis, with the 



r~ 



As 








\ 



'&uJ0>&~^ 




Fig. 232. — Acute Phthisis — Cavities formed by Softening of Areas of Coagulated 

Necrosis. 

changes in the lungs just described, within a short time the areas of 
coagulation necrosis soften and form cavities. Then the lung is 
honeycombed with irregular, ragged holes of different sizes (Fig. 232) . 



468 



THE RESPIRATORY SYSTEM. 



The conditions are the same as those seen in the rabbit's lung when 
infection with tubercle bacilli is followed by infection with strepto- 
cocci. It seems probable that in the human lung the softening of 
the areas of coagulation necrosis is due to a secondary infection 
with streptococci. 

Numerous observers have in fact found that the Streptococcus 
pyogenes is present often in enormous numbers both in the consoli- 
dated areas and in the walls of the cavities in acute phthisis in man. 

It is probable, furthermore, that in this concurrent infection with 




Fig. 233.— Acute Phthisis— Tuberculous Inflammation of the Lung and Dilatation of 

Bronchi. 



the tubercle bacillus and the streptococcus the latter may play a most 
important part not onl} T in the local lesion, but in the systemic poi- 
soning of which the hectic fever is so frequent a symptom. 1 

V. There are cases of acute phthisis in which the changes in the 
walls of the bronchi are especially marked, (a) The walls of the 
small and larger bronchi are infiltrated with tubercle tissue which 
undergoes cheesy degeneration. The cavity of the bronchus is 
dilated and contains inflammatory products also in a condition of 

1 Citation of the earlier studies on concurrent or mixed infection in pulmonary 
tuberculosis will be found in the study by Prudden, New York Medical Journal, 
July 7th, 1896. Consult also Petruschky. 



THE RESPIRATORY SYSTEM. 



469 



cheesy degeneration (Fig. 233). The adjacent air spaces may be 
unchanged, or may contain tubercle tissue, pus, fibrin, or epithelium. 
The necrosis may extend to the surrounding lung. In this way, 
partly by dilatation, partly by necrosis, cavities of considerable size 
-are formed. 

(b) There is a general dilatation of the bronchi in a considerable 
portion of the lung without any marked change in their walls, and 




Fig. 234.— Chronic Phthisis, x 850 and reduced. 
An air vesicle filled with fatty epithelium. 

with only a moderate quantity of inflammatory products in their 
cavities. This change is especially apt to affect the medium-sized 
and small bronchi. The lung tissue between the bronchi is usually 
•consolidated. When such a lung is cut it looks as if it were honey- 
combed with small cavities, but these cavities are only sections of 
the dilated bronchi. 

Chronic Pulmonary Phthisis. — The lesions are of the same 



4?0 



THE RESPIRATORY SYSTEM. 



iL2±ljjJJ^^ iiL hj ®^® 



^^^^g| 



Fig. 235.— Diffuse Tuberculous Inflammation producing Diffuse Consolidation of the 

Lung, X 300 arid reduced. 




Fig. 236.— Chronic Phthisis -Tntra-alveolar Pneumonia. 



THE RESPIRATORY SYSTEM. 



471 






m^Ck 




"' { ^M^ 



Fig. 237.— Chronic Phthisis, X 850 and reduced. 
Showing growth of connective tissue within an air vesicle. 




Fig. 238 —Chronic Phthisis, x 850 and reduced. 
Showing growth of connective tissue within an air vesicle. 



472 THE RESPIRATORY SYSTEM. 

nature as those of acute phthisis, but are modified by the long con- 
tinuance of the inflammation. 
1. The air spaces: 

(a) The air spaces are filled with swollen and fatty epithelium 
(Fig. 234), or with fibrin and pus, while their walls are unchanged 
and their blood vessels remain pervious. 

(b) The air spaces are filled and distended with compact fibrin and 
shrivelled pus and epithelium. Their walls are compressed and thin, 
or thickened and infiltrated with cells. The blood vessels can be only 

mm m ' ' / • / ,y ^ *> /"' W fflw 






w... 



t* 



Fig. 239.— Interstitial Pneumonia of Chronic Phthisis, X 850 and reduced. 

very imperfectly injected. This condition may be succeeded by com- 
plete cheesy degeneration. 

(c) The walls of the vesicles are thickened, their cavities are filled 
with new connective tissue often containing new vessels (Figs. 235, 
236, 237, and 238). This new connective tissue may look like an out- 
growth from the wall of the vesicle, or as if it was formed free in 
its cavity. 

(d) There is a diffuse interstitial growth of fibrous tissue and 
granulation tissue in the walls of the air spaces, the bronchi and the 
blood vessels, and in the septa. By this new tissue the air spaces 
are compressed and deformed or completely obliterated (Fig. 239). 



THE RESPIRATORY SYSTEM. 



473 



2. The nodules: 

These, as in acute phthisis, consist of areas of coagulation necro- 
sis, peribronchitic nodules, and miliary tubercles. 

The tubercles may preserve their characteristic structure, or un- 
dergo cheesy degeneration, or be changed into fibrous tissue (Fig. 
240). 

The areas of coagulation necrosis undergo cheesy degeneration, 
or soften and form cavities. They are surrounded by tubercle tis- 
sue, or granulation tissue, or connective tissue (Fig. 241). 



£*£?? ""A*, 7 " Tlr - ^ *^T 






Fig. 240.— An Old Miliary Tubercle converted ixto Fibrous Tissue ("Healed Tubercle ' , ), 

X 90 and reduced. 



The peribronchitic nodules are much the same as in acute phthisis. 
3. The bronchi : 

The changes in the bronchi in chronic phthisis form a very im- 
portant part of the morbid process. 

(a) The larger bronchi may be the seat of a chronic catarrhal 
inflammation, accompanied by the production of large quantities of 
mucus and pus. 

(b) The bronchi of all sizes may be inflamed, with the production 
of new cells in their walls, in addition to the inflammatory changes 
of their inner surfaces. Such a cellular infiltration of the walls of 
the bronchi is often followed by dilatation — either fusiform or saccu- 
lated. 

(c) Tubercle granula and granulation tissue are found in the 



474 



THE EESPIRATORY SYSTEM. 



walls of the bronchi. These tissues may degenerate, soften, and 
thus form ulcers. 

(d) The entire thickness of the wall of a bronchus may become 
the seat of inflammation of a peculiar character. The surface of the 
mucous membrane is coated with pus, the epithelial layer can no 
longer be seen, the wall of the bronchus is infiltrated with cells. 
The inflammatory products undergo cheesy degeneration, so that we 
find the inner surface of the bronchus coated with cheesy matter, 
while its wall is also changed into cheesy matter. Such a condition 
of the bronchus is usually followed by sacculated dilatation. 




© &M 



" _J ■••• '. 



mm w#^ 




-> „ ; ',$ \— „ r , v - , -4-1, ' * ;; <{ 







Fig. 241. -Tubercle Tissue around an Area of Coagulation Necrosis, X 850 and reduced. 

The cavities of chronic phthisis, therefore, are formed by the 
dilatation of inflamed bronchi, by the softening of areas of coagula- 
tion necrosis, or by the combination of both these processes. 

When cavities are once formed they are apt to continue and to 
become larger as the disease goes on. Their walls may be converted 
into granulation tissue, which ulcerates in some places and prolife- 
rates in others ; or portions of the wall become necrotic ; or all ac- 
tive processes cease and the wall of the cavity is formed of new 
connective tissue. The lung tissue between the cavities becomes 
compressed and altered in various ways. As the cavities increase in 



THE RESPIRATORY SYSTEM. 475 

size they touch and open into each other. In this way large portions 
of the lung may be converted into a dense mass honeycombed with 
cavities. 

VII. Syphilitic Pneumonia. 

Persons suffering from inherited or acquired syphilis sometimes 
develop inflammations of the lungs which seem to be due to the 
syphilitic infection. The lungs may then be affected in several dif- 
ferent ways. 




\ 






M 



Fig. 242— Interstitial Syphilitic Pneumonia, x 170 and reduced. 

1. There is an interstitial pneumonia, beginning around the lar- 
ger bronchi and blood vessels at the root of the lung, and extending 
to the walls of the air spaces and interstitial connective tissue, so that 
the central portions of one or both lungs are converted into a dense 
mass of connective tissue (Fig. 242). 

2. There is an interstitial pneumonia, with the formation of gum- 
my tumors. 

3. There is an inflammation of the wall of the trachea and of the 
larger bronchi. There are ulcers in the mucous membrane, their 
walls are very much thickened, and their cavities are narrowed or 
dilated. 

4. There are circumscribed areas of interstitial inflammation 



476 THE RESPIRATORY SYSTEM. 

around the smaller bronchi, forming small, hard peribronchitic 
nodules. 

5. There is a diffuse hepatization, involving lobules or an entire 
lobe. The affected portion of the lung is red or white or grayish. 
The walls of the air vesicles are infiltrated with cells, and their cavi- 
ties are filled with epithelial cells. 

6. There may be a broncho-pneumonia, like the ordinary broncho- 
pneumonia of children ; or a lobar pneumonia, like that of adults. 

7. There may be an obliterating endarteritis of branches of the 



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Fig. 243.— Primary Adenoma of the Lung, x 300 and reduced. 



pulmonary artery, with the formation of white infarctions sur- 
rounded by zones of connective tissue. 1 

TUMORS. 

Dermoid cysts have been found in the lungs in a few instances. 

Fibromata have been described by Rokitansky. 

Enchondromata may occur both as primary and secondary tu- 
mors. The primary tumors are small and are believed to originate 
in the cartilages of the bronchi. The secondary tumors often attain 
a very large size. 

1 Hitter, Cliarite Annalen, 1884, p. 184. 



THE RESPIRATORY SYSTEM. 477 

Osteoma is very rare. A case is described by Luschka. 1 

Sarcomata as secondary tumors are of not infrequent occurrence. 
A primary adeno-sarcoma is described by Weichselbaum. 2 

Lymphomata are found in cases of leukaemia and pseudo-leu- 
kaemia. 

Adenoma of the lungs is of rare occurrence as a primary tumor 
(Fig. 243). 

Carcinoma as a secondary growth, may have the form of nodules 
or of diffuse infiltration. Primary carcinoma of the lung has been 
described by a number of authors. The new growth is in the form 
of small nodules surrounded by pneumonia. As the result of the 
new growth and the pneumonia a considerable part of both lungs 
may be rendered solid. The bronchial glands may be infiltrated, 
and there may be secondary nodules in the pleura. 

The new growth may originate in the walls of the air spaces or in 
the walls of the bronchi. 3 

PARASITES. 

Echinococci occur in the lungs in their ordinary cystic form. 
The sacs may suppurate and discharge through the pleura, the 
bronchi, the wall of the chest, or the diaphragm. 

In bronchiectasiae and in gangrenous cavities in the lungs vege- 
table parasites of various kinds have been described — both moulds 
and bacteria. 

The Bacillus tuberculosis is regularly found in the walls and con- 
tents of cavities in acute and chronic phthisis, sometimes in enor- 
mous numbers. It is also often present in great numbers in the 
nodules of tubercular inflammation, particularly when these are 
softening and beginning to break down to form cavities (see Tuber- 
culosis). 

THE MEDIASTINUM. 

The anterior mediastinum is situated in front of the pericardium, 
between it and the sternum. At its superior part the two layers of 
pleurae separate somewhat to enclose the vestiges of the thymus 
gland ; behind the second piece of the sternum they are in contact, 
but below this the left pleura recedes from its fellow toward the 
left side, leaving an angular space of some breadth. The triangularis 
sterni muscle bounds this space in front. 

1 Virch. Archiv, Bd. x., p. 500. 

■ Ibid., Bd. lxxxv., p. 559. 

3 On the diagnosis of malignant tumors of the lungs, consult Betschart, Virch. 
Archiv, Bd. cxlii., p. 86, 1895; also Adler, New York MedicalJournal, February 
8th and 15th, 1896. 



478 THE RESPIRATORY SYSTEM. 

The posterior mediastinum, stretching from the pericardium to 
the bodies of the vertebrae, encloses between its layers the lower part 
of the windpipe and gullet, the thoracic duct, the descending aorta, 
the azygous vein, the pneumogastric nerve, and some lymphatic 
glands. 

INFLAMMATION. 

Suppurative inflammation may occur either in the anterior or 
posterior mediastinum. It may be caused by fractures, caries, or 
necrosis of the sternum and vertebrae, by perforation of the oesopha- 
gus, by suppuration of the lymphatic glands, by pleurisy, or may 
occur without discoverable cause. 

The pus may infiltrate the connective tissue, or may form ab- 
scesses which may attain a large size. The inflammation may ex- 
tend to the pleura or the pericardium , the abscesses may displace 
the heart, the lungs, or the sternum ; or they may perforate through 
the skin into a pleural cavity, the oesophagus, the trachea, or a 
bronchus. 

TUMORS. 

The most common form of new growth in the mediastinum is that 
known by the names of lymphoma, lympho-sarcoma, and lymph- 
adenoma. 

These tumors are confined to the mediastinum, or they are asso- 
ciated with similar growths in other parts of the body in the disease 
called ' ' pseudo-leukaemia. " 

Persons between the ages of twenty and thirty years seem to be 
the most liable to the growth, but it is also not uncommon in chil- 
dren. 

The growth begins in the lymphatic glands in the mediastinum, 
and at the root of the lung. It increases at first slowly, then more 
rapidly, and gradually infiltrates the adjoining tissues. In this way 
the walls of the trachea, bronchi, and aorta, the pericardium, the 
pleura, and the lung, become infiltrated with the growth. The tumor 
also compresses the surrounding organs. 

The growth is composed of a connective-tissue stroma infiltrated 
with small round cells, the relative quantity of cells and stroma vary- 
ing in the different cases. 

Besides this form of tumor there may also occur in the medias- 
tinum tumors similar to those which grow in the pleura and behind 
the peritoneum — tumors which resemble both the sarcomata and 
carcinomata, and which it is difficult to classify. Aberrant thyroid- 
gland tissue may be found in the mediastinum. 

Complex tumors belonging among the foetal inclusions or terato- 



THE RESPIRATORY SYSTEM. 479 

mata are of occasional occurrence in the anterior mediastinum. 
They may contain bone, cartilage, connective tissue, muscle, hairs, 
skin, etc. Cysts sometimes lined with ciliated epithelium may form 
in such tumors. J 

1 Consult Hare, " Tumors of the Mediastinum, " Philadelphia, 1889 ; also Zahn, 
Virchow's Archiv, Bd. cxliii., pp. 170 and 416, 1896. 



THE YASCULAK SYSTEM. 



THE PERICAEDIUM. 



INJURIES. 

The pericardium may be wounded by penetrating weapons, by 
gunshot wounds, and by fragments of bone. It may be ruptured 
by severe contusions of the thorax, and by rapid extravasation of 
blood into the pericardial sac. 

Perforations -may be produced by empyema, by mediastinal ab- 
scesses, by abscesses of the chest wall and of the liver, by aneurisms 
of the aorta, and by suppurative inflammation of the pericardium. 

DROPSY. 

In most post-mortems we find a little serum, from one-half ounce to 
one ounce, in the pericardial sac. This serum is usually clear and of 
a light-yellow color ; if decomposition has commenced it may be of a 
reddish color, or it may be slightly turbid from the falling-off of the 
pericardial epithelium. 

Large accumulations of serum are found as part of general drop- 
sy from heart disease, kidney disease, etc. The serum is clear and 
of a light-yellow color. Hydro-pericardium is usually moderate in 
comparison with the accumulations of serum in the other serous cav- 
ities ; sometimes, however, there is a very large amount of serum, 
which hinders the movements and interferes with the nourishment of 
the heart. 

HAEMORRHAGE. 

Extravasations of blood in the cavity of the pericardium are pro- 
duced by wounds and rupture of the heart, rupture of the aorta and 
of aneurisms, and occur with pericarditis. Small extravasations in 
the substance of the pericardium are found with scurvy, purpura, 
fevers, etc. 

PNEUMONATOSIS. 

Air or gas in the pericardium is sometimes found as a post-mor- 



THE VASCULAR SYSTEM. 481 

tern appearance, accompanied with drying of portions of the pericar- 
dium. 

Wounds or paracentesis of the pericardium ; the perforation of 
ulcers of the stomach, cavities of the lungs, and ulcers of the oeso- 
phagus, may admit air into the pericardial cavity. In purulent peri- 
carditis with foul, decomposing exudation, gases may be evolved. 

INFLAMMATION. 

Pericarditis is very rarely a primary lesion. It is most frequently 
associated with rheumatism and Bright's disease, but is also found 
with pneumonia, pleurisy, phthisis, endocarditis, pyaemia, and may 
be produced by injuries. 

The inflammations of the pericardium resemble those of the 
pleura. They usually begin acutely or subacutely, but may be- 
come chronic. There is a greater disposition to the escape of blood 
from the vessels than in pleurisy, so that the inflammatory products 
are often mixed with blood. The inflammatory process usually be- 
gins at the base of the heart and from there extends over the rest of 
the pericardium. 

Exudative Pericarditis. 

We may distinguish : 

1. Pericarditis with the Production of Fibrin. — In the milder 
examples of this form of pericarditis the pericardium is congested, or 
also studded with minute haemorrhages ; its surface is roughened by 
the deposition of a thin layer of fibrin. In the more severe cases the 
entire surface of the pericardium is covered with a thick layer of 
fibrin, and there are fibrinous adhesions between the visceral and 
parietal pericardium. If the inflammation continues for any length 
of time the pericardium itself becomes thickened and infiltrated with 
cells, and the wall of the heart may also undergo inflammatory 
changes. 

If the patient recovers the fibrin may be absorbed and the pericar- 
dium return to its normal condition. Or, instead of this, as the fib- 
rin disappears there is a growth of new connective tissue which 
forms permanent thickenings and adhesions of the pericardium, 
which may afterward become calcified. 

2. Pericarditis with the Production of Fibrin and a good deal 
of Serum. — In these cases the pericardium is coated with fibrin, but, 
in addition, there is a large effusion of serum into the pericardial sac. 
This serum accumulates at first between the floor of the pericardium 
and the lower surface of the heart, and, as it increases, distends the 
pericardial sac in all directions, pushing the heart upward and for- 
ward. The pericardial sac may be so much distended as to compress 

39 



482 THE VASCULAR SYSTEM. 

the trachea, the left bronchus, the oesophagus, or the aorta. If the 
patients recover the serum is absorbed, and permanent adhesions and 
thickenings are left. 

3. Pericarditis with the Production of Fibrin, Serum, and a 
good deal of Pus. — This variety may have the purulent character 
from the outset, or it may begin as one of the forms just described 
and afterward assume the purulent character. These latter cases 
are apt to run a chronic course. 

In the chronic cases the pericardial sac contains a large amount 
of purulent serum. The pericardium is coated with fibrin and is 
itself thickened and infiltrated with cells. The walls of the heart 



*■&& 



;#--«- 



1 ■'''■' ■•:,'."' _■-_: 

IT'ig^. 244.— Obliterature of the Pericardial Sac in a Child. 
Showing blood vessels growing from the visceral pericardium into the blood clot rilling the 
sac. Transverse section. A, Heart; B, pericardium; C, new-formed vascular tissue extending 
above to the unorganized clot. A similar layer of new vascular tissue was present over the 
parietal pericardium, and in places the two layers had coalesced, obliterating the sac. (Specimen 
loaned by Dr. Freeman.) 

may be the seat of interstitial myocarditis. In some cases the pro- 
ducts of inflammation undergo putrefactive changes ; in some cases 
the serum is absorbed and the fibrin and pus undergo cheesy degene- 
ration ; in some cases extensive connective-tissue adhesions and cal- 
cific plates are formed. 

The pathogenic bacteria most frequently found in the above va- 
rieties of pericarditis are the Streptococcus and Staphylococcus pyo- 
genes and the Diplococcus pneumoniae. 

Obliteration of the Pericardial Sac— As the result of the for- 
mation of vascular new connective tissue between the pericardial 
walls, the sac may be partially or wholly obliterated. 



THE VASCULAR SYSTEM. 483 

This may be the conclusion of an acute inflammatory process or 
ic may result from the organization of a blood clot (see page 73) 
following haemorrhage into the sac. It may occur as the result of 
the latter process early in life. 

Tuberculous Pericarditis. 

This lesion may occur by itself, but is apt to be associated with 
other tuberculous inflammation in the vicinity of the heart. There 
may be miliary tubercles scattered diffusely, or limited to certain 
regions in the pericardium, which is otherwise little changed. Not 
infrequently, however, there is a considerable thickening of the 
pericardium, either visceral or parietal, or both. 

In such cases the new-formed tissue consists of fibrous tissue and 
of tubercle tissue which has undergone extensive cheesy degeneration. 
The thickened visceral and parietal pericardium are often more or 
less grown together, so that the pericardial sac may be partially or 
almost completely obliterated. An inflammatory exudate often ac- 
companies the tuberculous process. 

TUMORS. 

Fibromata sometimes are developed in the pericardium. They 
are often of polypoid form, and from atrophy of the pedicle may be- 
come free in the pericardial sac. 

Sarcomata and carcinomata occur as secondary growths either 
from continuous infiltration or as metastatic tumors. 

Cysts of the visceral pericardium have been described. 

We have seen a pedunculated cyst, containing about 6 c.c. of 
clear fluid, hanging into the pericardial sac from its attachment near 
the pulmonary artery. The origin of these cysts is obscure. 

Endothelioma. — There may be a growth of flat cells arranged in 
anastomosing tubules which look like lymphatics, in the pericar- 
dium, resembling similar growths in the pleura. 



THE HEART. 
MALFORMATIONS. 

The malformations of the heart are usually closely connected 
with malformations of the aorta and pulmonary artery. They de- 
pend on arrest of, or abnormal, development; on endocarditis, myo- 
carditis, thrombosis, or mechanical causes. 

I. The common arterial trunk is only partially, or not at all, 
separated into aorta and pulmonary artery. The divisions between 
the heart cavities are at the same time defective : 



484 THE VASCULAR SYSTEM. 

1. There is one ventricle and no auricle. 

2. There is one ventricle and one auricle. 

3. There is one ventricle and two auricles ; the aorta is alone or 
incompletely separated from the pulmonary artery. 

II. The trunk of the pulmonary artery or of the aorta is ste- 
nosed or obliterated, and from the obstruction to the current of blood 
the development of the septa between the heart cavities is pre- 
vented. 

1. The aorta, at its origin, or in the ascending portion of the 
arch, is stenosed or closed. The pulmonary artery gives off the de- 
scending aorta, and supplies the carotids and subclavians. The fora- 
men ovale remains open, or there is no septum between the auricles. 
The ventricular septum is also usually defective. The right ven- 
tricle is hypertrophied. 

2. The pulmonary artery is stenosed or closed. Its branches are 
supplied by the aorta, through the ductus arteriosus. The ventricu- 
lar septum is defective, the foramen ovale is open, or the auricular 
septum defective. 

III. The malformation affects the aorta and pulmonary artery 
after they are more fully developed. 

1. There is stenosis of the aorta between the left subclavian and 
ductus arteriosus, or just at the opening of the ductus arteriosus. 
The descending aorta is then a continuation of the pulmonary 
artery. 

2. The aorta gives off all its branches from the arch, but the de- 
scending aorta is a continuation of the pulmonary artery ; or the 
carotids may spring from the aorta, the subclavians from the pul- 
monary artery. 

3. The vessels are transposed ; the pulmonary artery arises from 
the left, the aorta from the right ventricle ; the pulmonary veins 
empty into the left, the venae cavse into the right auricle ; or the 
veins also may be transposed. The septa are defective. 

IV. The aorta and pulmonary artery are normal, but the cardiac 
septa are defective. 

1. The foramen ovale remains partly open. This condition may 
continue through life without giving any trouble. 

2. The ductus arteriosus may remain open for many years ; this 
also may cause no disturbance. 

3. There is a small or large opening in the ventricular septum. 
This may give rise to no symptoms, unless disease of the heart or 
lungs be superadded. 

Y. Either of the auriculo-ventricular orifices may be entirely 
closed. The foramen ovale remains open, and the ventricular sep- 
tum is defective. 



THE VASCULAR SYSTEM. 485 

VI. The valves of the different orifices of the heart may be ab- 
sent or defective. The arteries or the ventricles are usually defec- 
tive at the same time. 

The aortic and pulmonary valves may consist of two large or 
four small leaves, instead of the usual three. The edges of the 
semilunar valves may be fenestrated. These alterations are usually 
of no significance. 

Generally speaking, the existence of openings between the two 
auricles or the two ventricles, admitting some admixture of venous 
and arterial blood, produces no marked change in the circulation. 
If, however, the passage of the current of venous blood into the 
right heart is in any way interfered with, the consequences are very 
serious. Cyanosis is produced, the skin is of a bluish color, the 
small veins and capillaries are dilated, exudation of serum and 
hypertrophy of connective tissue take place, especially in the fingers 
and toes. 

Besides the malformations already mentioned we may find : 

Entire absence of the heart. 

Abnormal septa and chordae tendinese in the heart cavities. 

Abnormal shapes of the heart. 

Abnormal positions of the heart. 

(a) There is a smaller or larger defect in the walls of the thorax, 
so that the heart projects on the outside of the chest ; the pericar- 
dium is usually absent. 

(b) The diaphragm is absent, and the heart is in the abdominal 
cavity. 

(c) The heart is in some part of the neck or head ; this occurs 
only in foetuses very much malformed. 

(d) The heart is transposed, being on the right side. 

ABNORMAL SIZE OF THE HEART. 

(a) The heart may be abnormally large in connection with ob- 
structive anomalies of the great vessels. 

(b) The heart may be abnormally small (hypoplasia). This most 
frequently occurs, according to Yirchow, in chiorotic individuals and 
those who are the victims of the hemorrhagic diathesis. In these 
cases the aorta and other large arteries are apt to be unusually small 
and thin-walled. 

Very rarely two more or less perfect hearts are found in the same 
thorax. 

CHANGES IX POSITION. 

Changes in the position of the heart are congenital or acquired. 
The congenital malpositions have already been mentioned. 



486 THE VASCULAR SYSTEM. 

The acquired malpositions are caused by: 

1. Hypertrophy of the heart ; its long axis approaches the hori- 
zontal direction. 

2. Changes in the thoracic viscera. Emphysema of both lungs 
pushes the heart downward. Emphysema, pleurisy with effusion, 
or pneumothorax of one side pushes the heart to the other side. 
Pleurisy or chronic pneumonia, producing retraction of one side of 
the thorax, draws the heart to that side. New growths, aneurisms, 
and curvatures of the spine displace the heart in various directions. 

3. Changes in the abdomen. Accumulations of fluid and new 
growths in the abdomen, and tympanites, may push the heart up- 
ward. 

WOUNDS AND RUPTURES. 

Wounds of the heart are produced by penetrating instruments, 
by bullets, and by fragments of bone. The right ventricle is the 
more frequently wounded ; next the left ; rarely the auricles. 

The wound may penetrate into the cavities of the heart or only 
pass partly through its wall, or a bullet or the broken end of a weapon 
may be embedded in the wall. If the wound penetrate a cavity and 
be gaping, death may follow instantly and the pericardium be found 
filled with blood. If the wound be small and oblique, the blood may 
escape gradually and death may not ensue for several days. In rare 
cases adhesions are formed with the pericardium and the wound 
cicatrizes. Wounds which do not penetrate may cause death by the 
inflammation which they excite, or may cicatrize. 

Bullets and foreign bodies may become encapsulated in the heart 
wall and remain so for years. 

Ruptures of the heart wall occur in various ways : 

1. Severe contusions of the thorax may produce rupture, usually 
of one of the auricles. 

2. Spontaneous rupture occurs usually in advanced life. Rupture 
is most frequent in the left ventricle, and, in a considerable proportion 
of cases, near the apex. There is usually one rupture, but sometimes 
more. The rupture is usually oblique and larger internally than ex- 
ternally. The heart wall, near the seat of rupture, may be infiltrated 
with blood, or blood may infiltrate the subpericardial fat. The heart 
wall may be of normal thickness, or thin ; it is usually soft and in a- 
condition of fatty infiltration or degeneration. The rupture very 
frequently takes place when the patient is quiet. Death may b& 
almost instantaneous or may not ensue for several hours. 

Fatty degeneration leading to rupture of the heart may be gene- 
ral, or it is frequently circumscribed and due to obliterating endar- 
teritis, atheroma, thrombosis, or embolus of one of the coronary 
arteries, whereby a portion of the heart wall is deprived of nourish- 



THE VASCULAR SYSTEM. 487 

ment and degenerates. Or rupture of a branch of one of the coronary 
.arteries may induce rupture of the heart wall. Acute and chronic 
myocarditis, with or without the formation of abscess or cardiac 
aneurism, or the presence of tumors in the heart wall, or hydatids, 
may lead to the rupture. 1 

3. In very rare cases rupture is produced by stenosis of the aorta 
and dilatation of the heart cavities. 

4. Rupture of the papillary muscles and tendons may be produced 
by fatty degeneration or inflammatory or ulcerative processes. 

ATROPHY. 

Atrophy of the walls of the heart may be accompanied with no 
change in the size of its cavities ; or with dilatation (the same as pas- 
sive dilatation); or, more frequently, with diminution in the size of 
the cavities. 

The atrophy involves most frequently all the cavities of the heart, 
but may be confined to one or more of them. 

The muscular tissue appears normal, or brown from the presence 
of little granules of pigment in the muscular fibres, which are some- 
times present in large numbers — brown atrophy ; or the muscular 
fibres may undergo fatty degeneration ; or there may be an abnor- 
mal accumulation of fat beneath the pericardium ; or there may be 
a peculiar gelatinous material beneath the pericardium — this con- 
sists of fat which has undergone mucous degeneration. The heart 
may be so much atrophied as to weigh four ounces. 

The causes of atrophy of the heart are : 

1. It is a congenital malformation ; the heart of an adult then 
looks like that of an infant. 

2. Any chronic and exhausting disease, repeated hsemorrhages, 
•old age, typhus fever, dysentery, etc. , may produce atrophy. 

3. Chronic pericarditis, with large serous effusion, or with thick- 
ening of the pericardium, producing constriction of the coronary ar- 
teries. 

4. Stenosis, atheroma, calcification, or thrombosis of the coronary 
arteries may produce partial or total atrophy. 

5. Myocarditis, with fatty or fibrous degeneration. 

6. Mitral stenosis may cause atrophy of the left ventricle. 

HYPERTROPHY. 

All the cavities of the heart may have their walls hypertrophied, 
or the thickening may involve one or more. While the wall of a 

1 Consult Councilman, "On Sudden Deaths due to the Heart, " Boston Medical 
and Surgical Journal, November 9th, 1893. 



488 THE VASCULAR SYSTEM. 

ventricle is thickened, its cavity may retain its normal size — simjrte 
hypertrophy ; or be dilated — eccentric hypertrophy ; or it may be 
contracted — concentric hypertrophy. 

Care should always be exercised in judging of this condition, for 
a firmly contracted heart seems to have a small cavity and thick 
walls. The existence of such a condition as concentric hypertrophy 
is denied by some authors. Eccentric hypertrophy is the most com- 
mon form. Simple hypertrophy is not common, but may occur in 
connection with the atrophied kidneys of chronic diffuse nephritis. 
The muscle tissue in hypertrophied hearts is firmer and denser than 
normal, and is apt to have a darker color. Fatty degeneration may, 
however, be associated with it, giving the walls a lighter appear- 
ance. It is probable that the increase of tissue in the hypertrophied 
heart wall is the result of increase both in size and number of the 
muscle fibres. 

Hypertrophy of both ventricles increases both the length and 
breadth of the heart. Hypertrophy of the left ventricle (alone) in- 
creases its length. The apex is then lower and further to the left 
than usual. Hypertrophy of the right ventricle (alone) increases 
the breadth of the heart toward the right side ; but sometimes the 
right edge of the heart retains its normal situation and the apex is 
displaced to the left. "With large hypertrophy of both ventricles, 
the base of the heart may sink, so that its long axis approaches a. 
horizontal direction. 

Hypertrophied hearts may weigh from forty to fifty ounces, or 
even more. 

Hypertrophy of the heart may depend upon a variety of causes : 

1. Changes in the valves ; either insufficiency or stenosis in the 
valves leading from a cavity, and insufficiency in valves leading to a 
cavity, may induce hypertrophy of its walls. 

2. Obstruction to the passage of blood through the arterial sys- 
tem, as in atheroma and other diseases of the intima ; congenital or 
acquired stenosis of vessels, pressure of tumors, etc., on vessels ; 
certain forms of chronic diffuse nephritis, especially atrophied kid- 
neys, lead to hypertrophy of the left ventricle, and sometimes sec- 
ondarily to hypertrophy of the right ventricle. 

3. Obstruction to the passage of blood through the pulmonary 
artery by stenosis or by certain diseases of the lungs, particularly 
emphysema and chronic phthisis, may lead to hypertrophy of the 
right ventricle, and, secondarily, of the right auricle and left ven- 
tricle. 

4. Any cause, whether muscular or nervous, which increases the 
rapidity and force of the heart's contractions, may produce hyper- 
trophy. 



THE VASCULAR SYSTEM. 489 

5. Dilatation of the ventricles, from any cause, is frequently fol- 
lowed by hypertrophy. 

6. Pericarditis may produce hypertrophy by inducing softening 
and dilatation of the ventricles, or by leaving adhesions which ob- 
struct the heart's action. Chronic myocarditis also may lead to hy- 
pertrophy. 

Finally, for some cases of hypertrophy no satisfactory cause can- 
be found. Howard's table of 105 cases of cardiac hypertrophy 
shows its association with arterio-sclerosis in 59 per cent; with ne- 
phritis in 13.4 per cent; with valvular lesion in 12.4 per cent. 1 

It should be borne in mind that an increase in the amount of fat 
in and about the heart may make the organ appear larger, when 
there may be actually a considerable decrease in the amount of mus- 
cle tissue. 

DILATATION. 

Dilatation may be combined with hypertrophy — active dilata- 
tion ; or there may be no increase of muscle tissue, but a thinning 
of the walls proportionate to the dilatation of the cavity — passive 
dilatation. 

Either one or all of the heart cavities may be dilated, the au- 
ricles most frequently ; next the right ventricle ; least often the left 
ventricle. 

Active dilatation has been considered under hypertrophy. 

Passive dilatation may be produced by : 

1. Changes in the valves. Mitral or aortic stenosis or insuf- 
ficiency may produce dilatation of the auricles and right ventricle. 
Pulmonary stenosis or insufficiency may produce dilatation of the 
right auricle and right ventricle. Aortic insufficiency, with or 
without stenosis or mitral insufficiency, may produce dilatation of 
the left ventricle. Dilatations from these causes are often succeeded 
and compensated for by hypertrophy of the heart walls. 

2. Changes in the muscular tissue of the heart walls. Serous 
infiltration from pericarditis, myocarditis, fatty degeneration and in- 
filtration, atrophy of the muscle fibres, may all lead to dilatation. 

3. A heart which is already hypertrophied may, from degenera- 
tion of the muscle, become dilated. 

4. Acute exudative inflammations of the lungs and acute pleuritic 
exudations, by rendering a large number of vessels suddenly im- 
permeable to the blood current, may produce su dden stasis in the 
pulmonary artery and dilatation of the right heart. 

5. There are curious cases of acute and chronic dilatation of the 

1 Howard, jolins Hopkins Hospital Reports, vol. ill. , p. 265. 
40 



490 THE VASCULAR SYSTEM. 

ventricles for which no mechanical cause can be found and which 
are very fatal. 

DEGENERATIONS. 

Acute Degeneration; Parenchymatous Degeneration of the 
Heart Muscle. — This lesion frequently occurs in typhoid and typhus 
fever, pyaemia, erysipelas, and other infectious diseases, as well as" 
in the exanthemata, as a result of burns, and under a variety of 
other conditions. It is characterized by the presence in the muscle 
fibres of the heart of greater or less numbers of albuminous gran- 
ules of various sizes, most of them very small. They are not as re- 
f ractile as fat droplets, and are insoluble in ether, while swelling up 
and becoming almost invisible under the influence of acetic acid. 
Sometimes they are so abundant as to conceal the striations of the 
fibres. The degeneration is usually quite uniformly diffused through 




Fig. ^45,— Fatty Degeneration op the Heart Muscle. Teased. 

the heart, whose walls are softer than normal and of a grayish 
color. This lesion may be associated with or followed by fatty de- 
generation. 

Fatty Degeneration of the Heart Muscle. — This consists in the 
transformation of portions of the muscle fibres of the heart into fat, 
which collects in the fibres in larger and smaller droplets, sometimes 
few in number, sometimes so abundant as to entirely destroy or 
conceal the normal striations (Fig. 245). These droplets are soluble 
in ether, and remain unchanged on treatment with acetic acid. 
This degeneration is sometimes quite universal, but is more apt to 
occur in patches, giving the heart muscle a mottled appearance. 
This mottling may usually be best seen on the papillary muscles. 
The degenerated areas have a pale-yellowish color, and the muscle 
tissue is soft and flabby ; but when moderate or slight in degree the 
gross appearance may be little changed, and the microscopical ex- 
amination be necessary for its determination. This degeneration 
may lead to thinning of the walls, or to rupture of the heart, or to 



THE VASCULAR SYSTEM. 



491 



inability to fulfil its functions. It is not infrequently the cause of 
sudden death. 

It may be secondary to hypertrophy of the heart, to inflamma- 
tion of the heart muscle, or to pericarditis ; to disturbances of the 
circulation in the coronary arteries by inflammation, atheroma, etc. 
It may be due to deteriorated conditions of the blood in wasting dis- 
eases, excessive haemorrhages, exhausting fever?, leukaemia, etc., 
to poisoning with phosphorus and arsenic and to the toxins of mi- 
crobic origin developed in infectious diseases, such as diphtheria, scar- 
latina, typhoid fever, etc. 1 It may occur in otherwise apparently 
healthy persons. 

Fatty Degeneration of the Endocardium. — It is not uncommon 
to find, especially in elderly persons, fatty degenerations occurring 




Fig. 246,— Fatty Infiltration or Lipomatosis of the Heart. 
The lesion is excessive, the heart muscle being to a large extent atrophied. (The fat cells are 
represented in the drawing, for the sake of clearness, of relatively too large size.) 



in patches, especially on the valves, but also on the general endocar- 
dium. They may also occur in ill-nourished and anaemic individuals. 
Small, or even considerable, areas of fatty degeneration appear, as a 
rule, to be of little or no clinical significance. They are at least not 
inconsistent with perfect health. In these areas of fatty degenera- 
tion the connective-tissue cells are more or less completely filled with 
larger and smaller fat droplets. 

Amyloid Degeneration of the endocardium or the walls of the 

1 Consult Fiexner, Johns Hopkins Hospital Bulletin, March, 1894 ; also SeJiam- 
scJiin, Ziegler's Beitrage zur path. Anat. , etc., Bel. xviii., p. 64, 1895. 



492 



THE VASCULAR SYSTEM. 



"blood vessels and intermuscular connective-tissue septa is a not very 
infrequent, but usually not very important lesion. 

Hyalin Degeneration sometimes occurs. 

Calcification of the products of inflammation in pericarditis, or 
of connective-tissue membranes in chronic pericarditis, sometimes 
occurs, and in the latter case the heart may be more or less enclosed 
by a calcareous shell. The muscle fibres of the heart wall may,, 
though rarely, become densely infiltrated wit.h salts of lime. 

Fatty Infiltration or Lipomatosis of the Heart. — This lesion, 
which should be clearly distinguished from fatty degeneration, con- 
sists of an unusual accumulation of fat about the heart and between 
its muscle fibres (Fig. 246). 

The subpericardial fat, which may be present in considerable quan- 




Fig. 247 —Atrophic Pericardial, Fat. 
From young person dead of carcinoma of the stomach and peritoneum. Stained with osmic 
acid and teased. 

tity under normal conditions, may be so greatly increased in amount 
as to form a thick envelope enclosing nearly the entire organ. Some- 
times the accumulation of fat extends into the walls of the heart, 
between the muscles, causing atrophy of the latter, frequently to a 
very great extent, so that the function of the heart is seriously in- 
terfered with. This occurs sometimes in general obesity, or as a re- 
sult of chronic pericarditis, or in drunkards, or in debilitated or old 
persons. 

Atrophy of the pericardial fat tissue not infrequently occurs in 
persons emaciated by chronic disease, and then the usual situations 
of the fat are occupied by a tissue resembling mucous tissue in its 
gross characters. Microscopical examination shows that in this 
atrophic fat the fat cells have largely lost their contents, and the 



THE VASCULAR SYSTEM. 493 

whole tissue has undergone a partial reversion to its original embry- 
onic form (see Fig. 24?). 

Myomalacia. — When, through obliterating endarteritis, athero- 
ma, thrombosis, or embolus of a branch of the coronary arteries, the 
blood supply is cut off from a circumscribed portion of the heart wall, 
the tissue in the affected area may undergo fatty degeneration, lead- 
ing to rupture. Or, instead of extensive fatty degeneration, the 
muscle fibres may break down into a granular detritus and the con- 
nective tissue about them suffer retrograde metamorphosis, so that 
the whole affected area may be soft and yellowish-white or graj'ish 
in color. If, as not infrequently occurs, there is considerable extra- 
vasation of blood, the degenerated area may be of a dark-red color. 
Under these conditions the wall may rupture ; or acute inflammatory 
processes may occur; or the degenerated tissue may be gradually 
absorbed, and replaced by new connective tissue which gradually 
grows dense, shrinks, and assumes the characters of cicatricial tissue. 
This may occur in any part of the heart wall or in the papillary 
muscles, but is most common in the region supplied by the anterior 
coronary arteries. When the heart wail is involved the new-formed 
connective tissue may yield to the blood pressure from within and 
aneurism of the heart be formed. 

Impaired nutrition of a portion of the heart wall as the result of 
narrowing or obliteration of the coronary arteries or their branches 
is of great significance, whether it lead to such extreme lesions as 
those just described, or to fatty degeneration, or to atrophy of the 
muscle cells with a production of new connective tissue, because it is 
the dominant factor in many cases of sudden death. 

According to Sternberg 1 the right coronary artery supplies the 
following regions of the heart: most of the right auricle; the poste- 
rior part and most of the anterior part of the right ventricle ; most 
of the interauricular and interventricular septa; the posterior part 
of the left ventricle and the posterior papillary muscles. The re- 
mainder of the heart is supplied by the left coronary artery. 

Fragmentation of the Myocardium. — Attention has been called 
by a number of observers to a condition of the heart muscle sometimes 
observed, it is said, in acute infectious diseases, in acute and chronic 
diseases of the central nervous system, and in sudden death from a 
variety of causes. The muscle tissue is soft, friable, opaque, and 
often yellowish. Examination shows a loosening of the muscle cells 
from one another, as if by some change in the cement substance. 2 It 
is still questionable whether this may not be a post-mortem change. 

1 Inaug. Diss., Marburg, 1887. 

2 Oestreich, Virchow's Archiv, Bd. cxxxv., p. 79, bibliography; also Dunin, 
Ziegler's Beitrage zur path. Anat., etc., Bd. xvi., p. 134, 1894. 



494 THE VASCULAR SYSTEM. 

INFLAMMATION. 

Endocarditis. 

The endocardium is a connective-tissue membrane which lines 
the cavities of the heart and forms its valves. Its inner surface is 
covered with a layer of endothelial cells. It is but poorly supplied 
with vessels, and the inflammations which attack it are of the cel- 
lular variety. The ordinary products of inflammation, pus, fibrin, 
and serum, are scanty or absent altogether. The connective-tissue 
cells and basement substance are principally concerned in the inflam- 
matory processes. The new tissue thus produced is prone to de- 
generation and calcification. The roughening of the endocardium 
due to the inflammation often causes a coagulation of fibrin on the 
inflamed surface. 

In foetal life it is the endocardium of the right heart, in extra- 
uterine life that of the left heart, which is usually inflamed. 

The endocardium which forms the valves is that which is most 
frequently inflamed, but the other portions of it are by no means 
exempt. 

1. Simple Acute Endocarditis. — This is most apt to occur in 
connection with rheumatism, but may occur under other conditions. 
It may attack a heart which was previously healthy, or one in 
which the lesions of chronic endocarditis already exist. 

In some cases the only lesion is a simple swelling of the valves. 
They are thick and succulent, but their surfaces remain smooth. 
The basement substance is swollen, and there is a moderate pro- 
duction of new connective-tissue cells. 

In other cases the growth of connective-tissue cells is very much 
more marked, the basement substance is split up, and little cellular 
fungous masses, called vegetations, project from the free surface of 
the endocardium. On these roughened surfaces the fibrin of the 
blood is deposited, and so vegetations of considerable size may be 
formed (see Fig. 248). 

In still other cases the cell growth, while in some places it forms 
vegetations, in other places degenerates, and thus portions of the 
valves are "destroyed. This is simple acute ulcerative endocar- 
ditis. 

In some cases of this disease the patients recover and the valves 
seem to return to a normal condition ; in other cases the valves are 
left permanently damaged ; and in still others chronic endocarditis 
follows the acute form. 

2. Mycotic or Malignant Endocarditis (malignant ulcerative 
endocarditis). 

The direct inciting cause of simple acute endocarditis of the forms 



THE VASCULAR SYSTEM. 495 

described above is unknown. But in a considerable number of cases 
of acute endocarditis bacteria have been found in and about the 
vegetations (see Fig. 249), and proved, by careful experiments, to 
stand in a causative relation to the lesion. 

Those cases of acute endocarditis in which the lesions are in- 
duced by the direct action of bacteria are called mycotic or malig- 
nant endocarditis ; or, since the new-formed as well as the old 
tissue about the bacteria is apt to become necrotic and thus lead to 
larger or smaller losses of substance, the lesion is often called ulcera- 
tive endocarditis. Cases of multiple aneurism in connection with 
mycotic endocarditis have been reported. 

Cultivations of the bacteria occurring in the heart lesions in 




Fig. 248.— Vegetation on Aortic Valve in Endocarditis. 
Showing granular thrombus over the surface. 

malignant endocarditis have shown that, while various species of 
bacteria may occasionally act as an inciting cause, it is most com- 
monly induced by the Staphylococcus pyogenes aureus and the Strep- 
tococcus pyogenes. The Diplococcus lanceolatus, B. typhosus, B. 
tuberculosis, B. anthracis, Micrococcus gonorrhoeae and others have 
been occasionally found. 

It has been, furthermore, found that a lesion or injury of the en- 
docardium, either on the heart valves or elsewhere, predisposes to the 
lodgment and growth upon them of the disease-producing bacteria 
when once they have gained access to the circulating blood. 1 

1 For a detailed consideration of the relationship of bacteria to malignant endo- 
carditis, with experiments and literature, see Prudden, Am. Jour. Med. Sciences, 
January, 1887; Weichselbaum. Ziegler's Beitrage zur path. Anat.. Bd. iv., 1888, 
p. 127 ; Thayer and Blume. Bull. Johns Hopkins Hospital, April, 1896. 



496 



THE VASCULAR SYSTEM. 



Mycotic endocarditis is frequently a secondary complicating le- 
sion, but may occur as a primary disease. It is most apt to be asso- 
ciated with the acute infectious diseases, and in many cases may be 
regarded as one of the local manifestations of pyaemia. 

In some cases there is a formation of new tissue in the form of 
organized vegetations on the valves or general endocardium ; in 
other cases necrosis either of the new-formed or the old tissue is the 
most marked feature. Blood clots are apt to form on the affected 
surfaces and often largely make up the so-called vegetations. The 
mitral and aortic valves are frequently the seat of the lesion, but it 
may occur elsewhere. 

Detachment of bacteria containing fragments of the vegetations 
or clots may give rise to single or multiple infectious emboli (see p. 
73) and abscesses in various parts of the body, such as the spleen, kid- 







Fig. 249.— Mycotic Endocarditis. 
Schematic drawing of a section of vegetation, showing colonies of micrococci stained with 
methyl violet. 

neys, brain, skin, heart wall, etc. Bacteria similar to those in the 
heart lesion may be found in these secondary abscesses (see Fig. 
6Q). 

It is probable that these abscesses in ulcerative endocarditis do 
not always arise from cardiac emboli, but may precede the heart 
lesion. 

3. Chronic Endocarditis may succeed acute endocarditis, or the 
inflammation may be chronic from the outset. It affects most -fre- 
quently the aortic and mitral valves, and the endocardium of the left 
auricle and ventricle • similar changes in the right side of the heart 
being much less frequent. 

There are two main anatomical varieties of chronic endocarditis, 
which may occur separately or together. 

(1) The endocardium is thick and dense, its surfaces are smooth 
or covered with small, hard vegetations or ridges ; it is Often infil- 
trated with the salts of lime. (Fig. 251). 



THE VASCULAR SYSTEM. 



497 



(2) There is a growth of connective-tissue cells in the endocar- 
dium, with a splitting-up of the basement substance. Some of the 
new cells continue to live, others degenerate. By the combination 
of such a cell growth and destruction the endocardium is in some 
places destroyed, in others changed into projecting vegetations. 
Fibrin is deposited on the roughened surfaces (Fig. 250) . After 
a time the condition may be further complicated by the shrink- 
age and deposition of the salts of lime in the new tissue and 




Fig. 250.— Chronic Endocarditis. 
Showing " vegetation " on heart valve with large blood clot— mitral valve. 

in the endocardium. All these changes may extend to the wall of 
the heart beneath the endocardium. 

The most important result of chronic endocarditis is its effect on 
the heart valves, producing insufficiency and stenosis. The changes 
in the valves are followed by changes in the walls and cavities of the 
heart, and disturbances of the circulation throughout the body. 
41 



498 



THE VASCULAR SYSTEM. 



4. Chronic Ulcerative Endocarditis. — Large ulcers or perfora- 
tions of the valves may be formed in chronic endocarditis, upon 
which clots may form, so that in gross appearance a great similarity 
exists between this and malignant ulcerative endocarditis, particu- 
larly if the latter have been engrafted upon an already chronically 
diseased endocardium. The microscopical and biological examina- 
tions must usually be resorted to in order to determine the exact sig- 
nificance of the lesion. 

5. Tuberculous Endocarditis may occur in connection with tu- 
bercular pericarditis or general miliary tuberculosis. The tubercles 




M 






Fig. 251.— Chronic Endocarditis. 
Thickening of the aortyc valve. 

may be small and single, or grouped in masses, and show the usual 
degenerative changes. 

Myocarditis. 

The inflammatory changes in the walls of the heart involve pri- 
marily the interstitial tissue and blood vessels, the muscle fibres 
being secondarily affected by atrophic and degenerative changes. 

Interstitial Myocarditis may be acute and purulent, or chronic 
with the formation of new connective tissue. 

Acute Purulent Myocarditis may be diffuse, infiltrating the 
wall of the heart with pus. This may occur as a complication of 
scarlatina and from unknown causes. 

More frequently the purulent inflammation is circumscribed, pro- 
ducing abscesses. These occur with pyaemia, mycotic ulcerative en- 



THE VASCULAR SYSTEM. 499 

docarditis, and other infectious diseases. They are of different 
sizes and either single or multiple. They are produced by the lodg- 
ment of infectious emboli in small vessels. The contents of the ab- 
scesses consist of pus, broken-down muscle tissue, and bacteria. 
These abscesses may open into the pericardial sac and set up a pu- 
rulent pericarditis ; or into a heart cavity, giving rise to thrombi in 
the heart and emboli in different parts of the body ; or the wall of 
the heart is weakened by the abscess so that it ruptures, or an aneu- 
rismal sac is formed ; or an abscess in the interventricular septum 
may establish an opening between the ventricles ; or the suppura- 
tive process may extend upward and form an abscess in the connec- 
tive tissue at the base of the heart. 

In rare cases the patients recover, the contents of the abscesses 
become dry and hard, and enclosed by a wall of fibrous tissue. 



***&&¥& 



&**®»a£fe .€> 







Fig. 252,— Chronic Interstitial Myocarditis. 
Showing transverse section of a portion of a papillary muscle. 

Chronic Interstitial Myocarditis may be associated with chronic 
pericarditis or endocarditis or myomalacia, but in a large proportion 
of cases it occurs in connection with lesions of the coronary arteries. 
Occasionally, however, there is a formation of new connective tissue 
in the myocardium as well as in the endocardium without evident 
lesion of the coronary arteries or the above-mentioned conditions. 
There is a growth of new connective tissue or of granulation tissue 
between the muscular fibres, with atrophy and degeneration of the 
muscle. This growth may be in the form of circumscribed patches 
(Fig. 252), or diffused over a considerable part of the wall of the 
heart. Such an interstitial inflammation is often followed by dilata- 
tion of the cavities of the heart, by the formation of aneurisms of the 
wall of the heart, and of thrombi in the cavities of the heart. 

It is believed by many observers that the new connective tissue 
which develops in the heart in connection with atrophy of the muscle 
fibres, as a result of impaired nutrition due to a narrowing of the 



500 THE VASCULAR SYSTEM. 

lumen of the coronary arteries, is not in the stricter sense inflamma- 
tory in its nature, but is rather a fibrous hyperplasia, the new- 
formed connective tissue forming secondarily, to replace the muscle 
fibres which have atrophied. It is interesting in this connection to 
note that under these conditions the muscle fibres immediately be- 
neath the endocardium and close around the blood vessels where the 
nutritive supply is most abundant are often not atrophied, nor is the 
growth of connective tissue marked. 

Syphilitic Myocarditis is accompanied by the growth of con- 
nective tissue or granulation tissue in the wall of the heart between 
the muscular fibres. The pericardium and endocardium may also be 
thickened, and pericardial adhesions may be formed. Gummata of 
the heart are of rare occurrence. 1 

CHANGES IN THE VALVES. 

Fenestration of the valves is usually a change productive of no 
bad consequences. It occurs very frequently in the aortic and pul- 
monary valves. The valves may be thinner than usual, and close 
to their free edges are small slits extending from the centre to the 
attached edges of a leaf. 

Aneurisms of the valves are produced in two ways : 

1. They are the result of endocarditis. One of the lamellae of the 
leaf of a valve is destroyed, and the other lamella is converted into 
a sac filled with blood. These aneurisms are found in the aortic 
valve, projecting into the ventricle ; and in the mitral valve, project- 
ing into the auricle. Not infrequently the wall of the aneurism 
gives way, so that there is a rupture entirely through the valve. 

2. The entire thickness of a leaf of a valve is converted into a 
sac filled with blood. This occurs in the aortic, mitral, and tricus- 
pid valves ; its cause is unknown. 

Haemorrhage in the substance of the valves is sometimes found 
in very young children. It does not appear to have much clinical 
importance: 

ANEURISM OF THE HEART. 

Sacs filled with blood, situated in the walls of the heart and com- 
municating with its cavities, are formed in several different ways. 

1. In consequence of inflammatory processes in the endocardium 
and muscular tissue, a small or large portion of the wall is converted 
into fibrous tissue. The portion thus changed no longer resists the 
pressure of the blood from within, and is driven outward. Such a 
pouch may be a circumscribed sac communicating with, the heart 

1 For consideration of gonorrhceal myocarditis consult Councilman, Am. Jour. 
Med. Science, September, 1893. 



^ 



THE VASCULAR SYSTEM. 501 

cavity by a small opening, or may look like a dilatation of part of the 
ventricle. The wall of such an aneurism becomes thinner as the sac 
increases in size. It is composed of the endocardium, new fibrous 
tissue, visceral pericardium, and sometimes the adherent parietal 
pericardium. The walls may calcify, or rarely they become so thin 
as to rupture externally or into the right ventricle. The sacs may 
contain fluid blood or be filled up with fibrin. 

Such aneurisms are usually situated in the wall of the left ven- 
tricle ; rarely in that of the left auricle. If they are in the septum 
they may project into the right ventricle. They are usually single, 
but sometimes two or three are found in the same heart. 

2. Fatty degeneration of the heart wall may reach such a point 
that the wall yields and is pouched out into an aneurismal sac. 

3. Endocarditis and myocarditis, or fatty degeneration, may so 
soften a portion of the heart wall that the endocardium and part of 
the muscular tissue are ruptured and a ragged cavity is formed. 
This form of aneurism usually does not attain a large size, but soon 
ruptures externally and causes the death of the patient. 

THROMBOSIS OF THE HEART. 

It is very common to find after death, in the heart cavities, yellow, 
succulent, semi-translucent masses. They are most common and of 
firmest texture in persons who die of acute inflammatory diseases. 
They may adhere quite firmly to the walls of the heart, and may ex- 
tend in long, branching cords into the vessels. They are formed in 
the last hours of life and just after death. They have no clinical or 
pathological importance. 

Coagulations of the fibrin of the blood in the heart do, however, 
occur during life, and may exist for years. If the fibrin adheres to 
the valves in small masses these are called vegetations ; if it coagu- 
lates in the heart cavities in larger bodies they are called thrombi or 
heart polypi. 

Such thrombi are found in all the heart cavities. They form 
flattened masses firml} 7 adherent to the endocardium; or rounded 
bodies in the spaces between the trabeculse; or have a polypoid shape 
and are attached by a narrow pedicle, or very rarely are globular and 
free in the cavity of the auricle. 

They are usually found in connection with some valvular lesion 
which prevents the free circulation of blood through the heart. 

They are firm, dry, and of a whitish color ; they may soften and 
break down at their centres, so as to look like cysts filled with pus, or 
they ma} T calcify. They are usually entirely unorganized, consisting 
simply of fibrin, but may become organized. 

One of us (Delafield) has seen an organized thrombus in the heart 



502 THE VASCULAR SYSTEM. 

of a man, whose history was unknown, who was found dead in the 
street. 

Wilson presented before the New York Pathological Society, 
1892, a large thrombus of the auricle which was partly organized. 
Cases are reported of organized thrombi in the auricles, which were 
the seat of tuberculous inflammation, which sometimes does not in- 
volve the heart wail. 1 

Sometimes sarcomatous and carcinomatous tumors in different 
parts of the body are accompanied b} r the formation of thrombi in the 
heart cavities, which are composed partly of coagulated blood, partly 
of tissue like that of the primary tumor. 



Primary tumors in the heart are rare, but sarcomata, myxomata, 
fibromata, and lipomata may occur. Bhabdomyomata, probably 
congenital, may occur in the heart wall as circumscribed nodular 
masses. 3 A cavernous tumor of this kind has been described. Sec- 
ondary tumors, as a result of metastasis or of continuous growth 
from adjacent parts, are not very infrequent. These are usually 
carcinomata or sarcomata. Secondary chondromata have been 
observed. Syphilitic gummata may occur in the heart wall. 4 

PARASITES. 

Echinococcus sometimes occurs in the heart wall and may per- 
forate into the cavities. Cysticercus cellulosse has been observed. 

THE BLOOD VESSELS. 
ATROPHY AND HYPERTROPHY. 

Atrophy of the blood vessels may involve the entire trunk or 
some of its elements. It may occur as a part of general malnutrition 
of the body, or in connection with atrophy of particular organs, 
or as an accompaniment of various diseases of the vessels them- 
selves. 

Hypertrophy, which is especially seen in the arteries, may occur 
in the establishment of a collateral circulation upon the closure of 
arterial trunks; or it may occur as the result of increased blood pres- 
sure, as in some forms of hypertrophy of the heart. 

1 Kotlar, Rev. Centralblatt f. Bakteriologie, April 7th, 1894, p. 498. 

2 For bibliography of heart tumors consult Berthenson, Arch, de Med. exp. , vol. 
v., p. 386. 

3 Justi, Centralblatt f. path. Anat, etc., January 18th, 1896. 

4 Loomis, Am. Jour, of the Med. Sciences, October, 1895, bibliography. 



THE VASCULAR SYSTEM. 5Q3 



DEGENERATION. 



Fatty Degeneration. — This may occur in the walls of otherwise 
unaltered vessels, or in those which have undergone a variety of in- 
flammatory or degenerative changes. It may occur either in the in- 
tima or media, or both, and may be so extensive as to form a very 
prominent gross lesion, or so little developed as to require the micro- 
scope for its recognition. When marked, especially if occurring in 
the intima of large vessels, smaller and larger spots or stripes or 
patches may be seen, of a yellowish-white color, usually sharply cir- 
cumscribed, and sometimes smooth, sometimes roughened on the 
surface. It is most apt to occur in the aorta, but may be found in 
any of the vessels. In moderate degrees of the lesion we find on 
section that the cells of the intima contain fat droplets in greater or 
less number. When further advanced, not only are the cells crowded 
with fat droplets, but the intercellular tissue also may be more or less 
densely infiltrated with them. Sometimes the infiltration is so dense 
that the tissue breaks down, and there may be an erosion of the sur- 
face, forming a so-called fatty ulcer. When the media is involved 
the muscle cells contain fat droplets. It may lead to the formation 
of aneurism or to rupture of the vessels. 

Calcification usually occurs in vessels otherwise diseased, *and 
may involve either the intima or media. It consists in the deposi- 
tion of salts of lime either in the cells or intercellular substance. 
The lime may be in the form of larger or smaller granules or in 
dense translucent plates. 

Amyloid Degeneration, which may affect all the coats of the ar- 
teries, but especially the intima and media, will be considered under 
the lesions of the organs in which it most commonly occurs. 

Hyalin Degeneration may cause thickening of the intima of 
the blood vessels by its conversion into or infiltration with a homoge- 
neous material somewhat similar to amyloid (see page 84). Or it 
may involve the entire wall of smaller vessels, converting them into 
irregular lumpy cords. The lumen of vessels thus changed may be 
obliterated or occluded by thrombi. 

THE ARTERIES. 

INFLAMMATION. 

Acute Arteritis. 

Acute inflammation of the walls of the arteries is, in the major- 
ity of cases, the result of injury, or of an inflammation in the vicin- 
ity of the vessel, or of the lodgment within it of some foreign body 
of an irritating or infectious nature. The inflammatory process may 



504 THE VASCULAR SYSTEM. 

be largely confined to the inner layer cf the vessels — endarteritis; 
or it may commence in the outer layers— periarteritis ; or it may 
involve the entire wall. 

The blood vessels in the outer layers may be congested, the tissue 
cedematous and infiltrated with pus cells^ and the entire wall may 
become necrotic. The intima, if this layer is involved, loses its natu- 
ral gloss, looks dull and swollen. It may become infiltrated with 
pus from the outer layers, and it may become necrotic. Under these 
conditions thrombi usually form, and in these may occur the various 
changes which have been already described on page 60 

Chronic Arteritis. 

Since the publication of the studies of Gull and Sutton on arterio- 
capillary fibrosis, attention has been every year more and more di- 
rected to morbid changes in the arteries as one of the most frequent 
of diseased conditions. 

It is evident that these morbid changes are caused by alcohol, 
lead, gout, and syphilis; that the disposition to them is hereditary in 
some families ; that they constitute one of the regular senile changes ; 
that they are often associated with chronic diseases of the viscera ; 
that the patients can be unconscious of their existence, and that, on 
the other hand, they can cause most distressing symptoms, and even 
death. 

At the present time it is customary to speak of these morbid con- 
ditions under the names of arterio-sclerosis and atheroma, and to 
accept the conclusions drawn by Thoma from an extended series of 
studies. Thoma teaches that : 

1. Every long-continued slowing of the blood current causes con- 
traction of the middle coat of the aorta, and, if this is not sufficient 
to accelerate the blood current, to a growth of connective tissue in the 
intima. 

2. Primary diffuse and nodular arterio-sclerosis depends upon a 
weakening of the wall of the blood vessel due to constitutional con- 
ditions. This is followed by dilatation of the vessel, slowing of the 
blood stream, and then the growth of connective tissue in the intima. 

3. Secondary arterio-sclerosis is caused by slowing of the biood 
current produced by changes of the circulation in the capillary 
vessels. 

It appears to me (Delafield) that the most practical view of these 
morbid changes in the arteries is to consider them the results of a 
combination of chronic productive inflammation and of degeneration 
occurring in connective tissue. We shall then think of the arteries 
as we do of the heart or the liver or the kidneys, as a definite part 
of the body, liable to become the seat of chronic inflammation from 



THE VASCULAR SYSTEM. 505 

the same causes as those which produce similar changes on other 
parts of the body. 

In all the arteries the wall is composed of an outer connective-tis- 
sue coat supplied with blood vessels, of a middle coat formed of 
smooth muscle, and of an inner connective-tissue coat not supplied 
with blood vessels. In the small arteries inflammation simply causes 
the formation of new tissue ; in the large arteries and in the aorta, 
besides the formation of new tissue, there is also the death and de- 
generation of tissue. 

There is sufficient difference between the changes in the small 
arteries, the large arteries, and the aorta to make it convenient to 
described them separately. 




"*V 



Fig. 253.— Chronic Arteritis— Cerebral Artery. 
Inner coat thickened; degeneration and softening (atheroma) of a part of the thickened area. 

1. The Small Arteries. — («) The simplest change in the small 
arteries is an increase in the size and number of the endothelial cells. 
This is best seen in the arteries in miliary tubercles and in small 
gummata. 

(b) There is a growth of new connective tissue from the endothe- 
lium which encroaches upon the lumen of the artery and finally oc- 
cludes it. The growth is composed of large branching cells, small 
round cells, and basement substance ; later the cells become smaller 
and less numerous, the basement substance denser. The growth 
forms a ring on the inside of the intima which is not symmetrical, but 
is thicker in some one place. This change always narrows the calibre 



506 



THE VASCULAR SYSTEM. 



of the artery, and, when far advanced, occludes it. It is seen very 
frequently in the small arteries in every part of the body. It is often 
called "obliterating endarteritis" (Figs. 253 and 254). 

(c) There is a thickening of the inner coat beneath the endothe- 
lium. The change begins by a growth of cells and a splitting-up of 
the basement substance in the intima immediately beneath the endo- 
thelium. Then there is a growth of basement substance, with but a. 
moderate number of cells, which renders the inner coat thicker and 




Fig. 254.— Chronic Obliterating Endarteritis— Kidney. 

thicker until the lumen of the artery is considerably narrowed, but 
yet the artery is not occluded. The endothelial cells may remain in 
place and unchanged over the thickened intima. This change is of 
very frequent occurrence, so that it is easy to see all the stages of the 
growth, from the first splitting-up of the intima until it is changed 
into a dense thickening. 

(d) The thickening of the inner coat just described, instead of 
occurring by itself, may have joined with it either a thickening of 



THE VASCULAR SYSTEM. 507 

the muscular coat alone or a thickening of both the muscular and 
outer coats (Figs. 255 and 256) . 

(e) There is a thickening of the intima, a replacement of the mus- 
cular coat by connective tissue, and a thickening of the outer coat. 
This can properly be called a " sclerosis" of the artery. 

Periarteritis Nodosa,— A few cases have been described in 
which many of the small arteries in the muscles and in the viscera 
were beset with small* white knobs projecting from inside or sur- 
rounding the vessels. These circumscribed thickenings of the vessel 
wall are apt to involve all the layers of the vessel and may encroach 



. • :v. 




Fig. 255.— Chronic Arteritis. 
Inner and middle coat thickened— radial artery. 



upon the lumen. The thickened portions are infiltrated with small 
spheroidal cells. Multiple aneurisms may develop at the seat of 
the local thickenings. 1 

2. Tlie Large Arteries. — In the large arteries altogether the most 
frequent change is the thickening of the intima. This is often pres- 
ent in arteries which look normal to the naked eye. But besides the 
thickening of the intima there is often in addition a thickening of 

1 Consult?. RaMden, Ziegler's Beitrage z. path. Anat. , etc., Bd. xv., 1894; also 
Graf, ibid., Bd. xix., p. 181, 1896. 



508 



THE VASCULAR SYSTEM. 



the middle and outer coats, or a replacement of the muscular coat by 
connective tissue. When all the coats are thickened in this way the 
arteries often become elongated and tortuous. Occasionally there are 
areas of degeneration in the thickened wall of the artery, or even in- 
filtration with the salts of lime. 

The Aorta. — The changes in the aorta differ from those in the 
arteries by reason of the combination of degeneration and necrosis 
with the growth of new tissue due to the chronic inflammation, by 




M^ 




Fig. 256.— Chronic Arteritis. 
With sclerosis of all the coats of the vessel— kidney. 

the frequency of calcification, and by the liability of the outer coat to 
purulent infiltration. We find, therefore, in the aorta: 

(a) Simple thickening of the inner coat by new connective tissue. 

(b) Degeneration and softening of the inner and middle coats. 

(c) Calcification of the inner and middle coats. 

(d) Infiltration of the outer and middle coats with pus cells. 

(e) Thinning and atrophy of the inner and middle coats. 

(/) The formation of thrombi on the roughened surface of the 
inner coat. 



THE VASCULAR SYSTEM. 



509 



Inflammatory changes in the aorta associated with degeneration, 
calcification, etc., are often called "atheroma" (See Figs. 258 and 
259). 

Tuberculous Inflammation of the Arteries. 

In tuberculous inflammation the walls of the arteries, particularly 
the smaller ones, may be thickened and their lumina obliterated 
(Fig. 260). 





X 



Fig. 257.— Chronic Arteritis. 
With thickening of all the coats of the vessel— kidney. 



DILATATION AND ANEURISM. 

1. Cirsoid aneurism consists in the dilatation and lengthening 
of large or small arteries. The walls of the artery are thinned, the 
vessel is tortuous and in places sacculated. These changes are most 
frequent in small arteries, especially the temporal and occipital. 



510 



THE VASCULAR SYSTEM. 




Fig, 258.— Chronic Inflammation op the Aorta, with Degeneration of New-formed Tissue 

(Atheroma). 
a, adventitia; 6, media; c, new tissue developed iu the intima; d, degenerated area; e, area of 
softening; g, fat droplets in softened area. 







Fig. 259.— Chronic Inflammation of the Aorta. 
Inner coat thickened and necrotic; middle coat calcined, necrotic, and breaking down (atheroma). 



THE VASCULAR SYSTEM. 



511 



They involve the trunk of the vessel and its branches, or may extend 
to the capillaries and small veins. They form larger or smaller 
tumors beneath the skin. 

Rarely the} 7 are found in the larger arteries, and even in the aorta. 

2. The ordinary aneurism is a dilatation of the coats of the 
artery over a larger or smaller part of its course. Such dilatations 
are usually due to chronic endarteritis and atheroma. The blocking 




Fig. 



-Tuberculous Arteritis in the Lung. 



Showing the encroachment of an area of tuberculous inflammation upon the wall of the artery 
and the formation of a mass partly occluding the lumen of the vessel. This section shows how 
the generalization of the tubercular inflammation through the body may occur by the sweeping 
away of the tubercle bacilli by the blood and the establishment of new foci in various parts of the 
body. From specimen prepared by Dr. J. S. Ely. 

of a vessel by an embolus may lead to the development of an aneur- 
ism. According to their shape we may distinguish two varieties of 
aneurism : the diffuse and the circumscribed. 

(a) The diffuse, cylindrical, or fusiform aneurism consists in a 
uniform dilatation of all the coats of an artery, so that it assumes the 
shape of a fusiform or cylindrical swelling. In the walls of the 
dilated portion of the vessel there are often smaller, circumscribed 
dilatations. The wall of the aneurism is atheromatous or calcified ; 
the middle coat .may be atrophied. The arch of the aorta is the most 
common seat of this form of aneurism, but the entire length of the 
aorta, or parts of any other arteries, may be dilated in the same way. 



512 THE VASCULAR SYSTEM. 

(6) The circumscribed or sacculated aneurism consists either in a 
dilatation of the entire circumference of an artery over a short por- 
tion of its length, or in a dilatation of only a small portion of one 
side of the wall, so that the aneurism looks like a swelling attached 
to one side of the artery. The aneurism commences as a dilatation 
of all the coats of the vessel ; but as soon as it attains any consider- 
able size the middle coat atrophies, so that the wall is composed of- 
the inner and outer coats ; or the inner coat is destroyed by endar- 
teritis, so that the outer coat alone forms the wall of the aneurism. 
As the aneurism increases in size it presses upon and causes the de- 
struction of the neighboring tissues and viscera, and portions of these 
tissues and viscera become incorporated with, or take the place of, the 
wall of the aneurism. The cavity of the aneurism is filled with fluid 
or clotted blood, or with layers of fibrin which adhere closely to its 
wall. The communication between the aneurism and the artery may 
be small or large. If arterial branches are given off from the aneu- 
rism they may remain open or become plugged with fibrin ; or their 
walls are thickened and their cavities narrowed by endarteritis. 
Death is produced by the pressure and interference of the aneurism 
with the adjoining viscera, or by rupture. The rupture may allow 
enough blood to escape to destroy life, or the blood may be held in by 
the soft parts and a second false aneurism formed about the original 
one. 

Dissecting aneurisms are those in which, owing to a solution of 
continuity of the inner layers of the artery, the blood gets between 
the media and adventitia, and forces its way for a greater or less 
distance between them. Or it may separate the media into two 
layers. 

ANEURISMS OF THE DIFFERENT ARTERIES. 

The aorta may be dilated over its entire length, or there may be 
diffuse or circumscribed dilatations at any portion of its course ; or 
there may be several aneurisms, situated at different points. The 
ascending portion of the arch of the aorta may be uniformly dilated 
in a fusiform shape, or there may be circumscribed dilatations on its 
anterior wall, or, more rarely, on its posterior wall. The sacculated 
aneurisms may be of all sizes and may rupture within the pericar- 
dium ; or they may form a cavit}^ in the upper part of the ventricular 
septum and communicate by openings into the pulmonary artery and 
left ventricle ; or they may dilate downward between the visceral 
and parietal pericardium, in front of the heart, pushing that organ 
backward. They may perforate into the right or left auricle or right 
ventricle, the superior vena cava, or the pulmonary artery ; or they 
may reach a large size, press on and erode the right side of the 



THE VASCULAR SYSTEM. 513 

Sternum and adjoining ribs, project under the skin, and even rup- 
ture externally. 

The transverse portion of the arch may be dilated in a fusiform 
shape, or there may be sacculated aneurisms at any point in its wall. 
The sacculated aneurisms usually reach a considerable size. They 
press on the sternum and ribs in front, or on the oesophagus, trachea, 
and bronchi behind. The large arteries given off from the arch may 
be occluded. They cause death by pressure on the air passages, the 
oesophagus, and the vena cava ; or may rupture externally or into 
the oesophagus, trachea, bronchi, pulmonary artery, or pleural cavi- 
ties. 1 

On the abdominal aorta we usually find aneurisms sacculated. If 
they are situated high up they may project into the pleural cavities; 
if lower down, into the abdomen. They may compress and displace 
the viscera, vessels, and nerves, and erode the vertebrae. They may 
rupture behind the peritoneum, into the peritoneal cavity, the pleural 
cavities, the inferior vena cava, the bronchi, the lungs, the duodenum, 
the colon, the pelves of the kidney, or the posterior mediastinum. 

The coronary arteries may be dilated throughout, or may be the 
seat of small sacculated aneurisms. These may rupture into the 
pericardium, or may cause rupture of the heart wall. 

The pulmonary arteries are rarely the seat of aneurisms. Dif- 
fuse and circumscribed dilatations, however, sometimes occur on the 
main trunk and on the two principal branches of the artery. They 
do not usually reach a large size, but may cause death by rupture. 
General dilatation of all the branches of the pulmonary artery is 
more common. It is found in connection with stenosis of the mitral 
valves and with compression or induration of the lung tissue. 

Of the other arteries of the body there is hardly any one which 
vns.j not become the seat of an aneurism, but those of the popliteal 
artery are most common. 

A very few cases of multiple small aneurisms have been described, 
involving many of the smaller arterial trunks (see Periarteritis 
nodosa, 2 page 507). 

STENOSIS. 

Stenosis and obliteration of the aorta, at the point of entrance of 
the ductus arteriosus, have been described in a considerable number 
of cases. 

The situation of the stenosis is either exactly at the entrance of 
the ductus arteriosus or close on either side of this point. The de- 

1 For an analysis of thirty -four cases of aortic aneurism consult Biggs, Am. 
Jour, of the Med. Sciences, March, 1889. 

2 Graf, Ziegler's Beitrage zur path. Anat., etc., Bd. xix., p. 181, 1896. 

42 



514 THE VASCULAR SYSTEM. 

gree of stenosis varies. The aorta may be entirely closed and con- 
verted into a solid cord for a length of half an inch ; or there may 
be a circular constriction through which there is a larger or smaller 
opening — the constriction is uniformly circular ; or there is a septum 
springing from the concave side of the vessel at the opening of the 
ductus arteriosus ; or there is a cicatricial-like contraction of the aorta. 
The walls of the aorta at this point may be thickened and sclerosed. 
The ductus arteriosus may be closed or open. Above the constriction 
the aorta is usually dilated ; below it, it is normal, dilated, or ste- 
nosed. 

Stenosis of the aorta produces hypertrophy of the left ventricle, 
and, later, of the right ventricle, with venous congestion through- 
out the body ; or there may be a collateral circulation developed be- 
tween the arteries given off above and below the constriction ; or 
there may be rupture of the aorta, the right ventricle or auricle. 

This condition is found at all ages, but is produced during foetal 
life or in the first year of extra-uterine life. It is probable that it 
may be caused after birth by an abnormal closure of the ductus ar- 
teriosus. This vessel normally becomes closed without the forma- 
tion of a thrombus. If a thrombus is formed it may extend into the 
aorta and obstruct it ; or the ductus arteriosus is filled with a throm- 
bus, but increases for a time in size ; afterward, as the thrombus is ab- 
sorbed, the vessel contracts and draws the walls of the aorta together. 

Stenosis of the aorta and of some of the other arteries has been 
observed, in a few rare cases, without any known cause. 

Endarteritis, with the production of atheromatous and calcareous 
patches, may obstruct or entirely obliterate the smaller arteries. 
This is especially seen in the arteries of the leg, foot, and brain, and 
in the coronary arteries. The writer has seen a case in which the 
subclavian was completely occluded in this way. 

Narrowing of the aorta and of all its branches, with thinning of 
the arterial coats, is found as a congenital condition. It usually oc- 
curs in females, in connection with imperfect development of the 
whole body. 

Stenosis from thrombosis or embolism is treated of elsewhere. 

RUPTURES AND WOUNDS. 

Rupture of arteries may occur under the following conditions : 
1. Fatty degeneration or endarteritis, with atheromatous changes, 
may so soften and destroy the inner and middle coats of an artery as 
to admit of its rupture. Rupture of the aorta in connection with 
tuberculous inflammation of the vessels has been described. The 
aorta, just above the valves, is the most frequent seat of this lesion. 
The rupture may run in any direction; its edges are irregular and 



THE VASCULAR SYSTEM. 515 

jagged. The blood may burst through all the coats of the aorta at 
the same point ; or more frequently the external coat remains and 
the blood is infiltrated in the middle coat and between it and the 
external coat. In this way a dissecting aneurism is formed, which 
may extend along the aorta for a considerable distance. After a 
short time the external coat usually gives w T ay at some point, and the 
blood escapes. In rare cases life is prolonged for some time, the 
rupture being closed by a new membrane. 

We also find ruptures from fatty degeneration and atheroma in 
the arteries of the brain and lungs ; in the coronary arteries, the 
coeliac axis, the mesenteric arteries, and in the arteries of the ex- 
tremities 

2. In rare cases stenosis of a portion of the aorta may cause 
rupture at some point betAveen the seat of stenosis and the heart. 

3 Contusions, Avrenchings, and seA^ere falls may rupture the 
Avails of an artery, either partially or completely, producing trau- 
matic or dissecting aneurisms, or completely severing the vessel. 

4. Penetrating wounds may injure or entirely seA^er an artery. 
If the A T essel be large and the injury severe, death from haemorrhage 
is the usual result. A small artery may become closed or be the seat 
of a false aneurism. 

In the healing of a Avounded artery tAVO conditions co-operate. 
The A^essel retracts and contracts, and a thrombus is formed Avithin 
it. The contraction may be alone sufficient to close the A T essel ; its 
coats thicken, and the inner surfaces finally are fused together ; or 
the blood coagulates and forms a thrombus in the vessel near the 
Avound. This thrombus later becomes organized and the A r essel is 
coiiA^erted into a fibrous cord. 

Spurious or false aneurisms are found most frequently con- 
nected AA T ith vessels of the extremities. When an artery is wounded 
the blood escapes into the surrounding soft parts, and a cavit} T is 
formed filled Avith blood and broken-down tissue. This condition 
may terminate in several Avays. 

(a) The wound in the artery may heal and the effused blood be 
absorbed. 

(b) The effused blood and broken tissues may become gangrenous 
and the surrounding soft parts be inflamed. 

(c) A sort of sac wall may be formed by the soft parts, Avhile the 
wound of the artery remains open, so that Ave have an aneurismal 
sac through which the blood is constantly pouring. 

5 If an artery be Abounded, and at the same time the A r ein Avhich 
accompanies it, Ave haA^e as the result the conditions called aneu- 
rismal A^arix and varicose aneurism. In aneurismal varix the artery 
and A^ein become adherent at the seat of injury., so that the arterial 



516 THE VASCULAR SYSTEM. 

blood passes directly into the vein. There is a smooth, rounded 
opening between the two vessels, the vein is dilated into a sac, and 
the veins emptying into it are dilated and tortuous. 

In varicose aneurism the artery and vein do not communicate di- 
rectly, but a false aneurismal sac is formed between the vessels, into 
which the blood is poured before passing into the vein. 

Varicose aneurism may also be produced by the spontaneous rup- - 
ture of an aneurism into a vein. The aneurism presses against the 
vein, becomes adherent, and finally ruptures into it. This condition 
has been observed between the aorta and pulmonary artery ; the aorta 
and inferior and superior vena cava ; the popliteal artery and vein ; the 
femoral artery and vein ; the splenic artery and vena azygos ; the in- 
ternal carotid and sinus cavernosus. Even in cases of perforation 
by aortic aneurisms life is usually prolonged for some time. 

6. Destructive inflammation or tumors of the surrounding tissues 
may invade and destroy a portion of the wall of an artery. Thus 
ulceration of the trachea, bronchi, bronchial glands, and oesophagus, 
or tumors of these parts, may perforate the aorta ; gangrene of the 
lungs, the pulmonary arteries; ulcer of the stomach, the gastric 
arteries, etc. 

TUMORS. 

Secondary tumors, chiefly carcinomata and sarcomata, may occur 
in the walls of the arteries by continuous growth from without, 
involving first the external layers. To these layers they are usually 
confined, for the density of the inner layers affords such marked 
resistance to the infiltration of the tumor cells that they are apt to 
pass intact through the tumor, which grows around them. More 
frequently the arteries become secondarily involved in the growth 
of malignant tumors by the occurrence within them of emboli 
formed by larger and smaller masses of tumor cells. 

These emboli are usually of small size, and are apt to get into the 
circulation by growing through the walls of the veins into their lu- 
mina. Large emboli from tumors are most apt to occur in the branches 
of the pulmonary artery. The emboli, formed as they are for the 
most part by cells capable of growth and proliferation, are apt to soon 
form connection with the walls of the vessels, and, by the growth 
into them of blood vessels from the vasa vasorum to find the condi- 
tions necessary for their development, and they may thus soon in- 
volve the entire wall of the vessel and grow out into adjacent parts. 



THE VASCULAR SYSTEM. 517 

THE VEINS. 
DILATATION. 

Dilatation of the veins, or phlebectasia, presents itself under a va- 
riety of forms. 

1. Simple Dilatation. — The vein is uniformly dilated in a cylin- 
drical or fusiform shape ; its length is not increased ; its walls are of 
normal thickness or thinned ; the valves increase in size, or are in- 
sufficient, or atrophic, or are torn. 

2. Cirsoid Dilatation. — The vein is uniformly cylindrically di- 
lated, but is also increased in length, so that it assumes a very tor- 
tuous course. The walls are normal, thickened, or thinned. 

3. Varicose Dilatation. — A circumscribed portion of the wall of 
the vein is dilated so as to form a globular sac. The sac communi- 
cates with the vein through a large or small opening. The wall of 
the sac is formed of the coats of the vein, which preserve their nor- 
mal thickness, are thickened or thinned ; the middle coat may dis- 
appear entirely. There may be only one such dilatation, or there 
may be a number on the same vein, or a number of veins may be af- 
fected at the same time. The vein may be otherwise normal, or, 
more frequently, is dilated in the cirsoid form. 

4. Anastomosing Dilatation. — A number of contiguous and 
anastomosing veins are dilated, both in the cirsoid and varicose 
forms. The vein then looks like a series of cavities separated by 
thin partitions. The dilatations of the same vein become adherent 
to each other and to those of the adjoining veins ; portions of the 
wall of the dilated parts may disappear, and we find a number of 
cavities containing venous blood and separated from each other by 
thin partitions. The course of the vein can no longer be followed 
out. 

Spontaneous cure of dilatations of the veins is not common, and 
usually occurs only in the lesser degrees of the lesion. Most phle- 
bectasiae increase steadily in size and extent. Very frequently 
thrombi form in the dilated veins, and either partially or completely 
fill them ; and these in rare cases may become organized, or the 
clots may dry and become calcified, forming phleboliths (see page 
60), and, by the formation of new connective tissue in the walls, 
they may become enclosed in a fibrous capsule, with the oblitera- 
tion of the vessel. The wall of the dilated sac may become so thin 
that it finally ruptures, and the blood is discharged externally. 
Sometimes inflammation is set up in the tissues surrounding the 
vein, and we find both the surrounding tissues and the wall of the 



518 THE VASCULAR SYSTEM. 

vein the seat of purulent infiltration or fibrous thickening. The 
parts of the body from which the dilated veins draw their blood may 
exhibit the results of chronic venous congestion, oedema, hyperemia, 
and hypertrophy or ulceration. 

When occurring in mucous membrane, dilated veins are usually 
associated with persistent catarrh. There is hardly one of all the 
veins of the body which may not be dilated. The hsemorrhoidal 
veins ; the veins of the leg and thigh ; those of the pelvis and pelvic 
viscera ; those of the spermatic cord, scrotum, and labia ; those of 
the abdominal wall ; those of the neck and arms — are the ones most 
frequently found in this condition. 

The causes of dilatation are principally some mechanical obstruc- 
tion to the passage of the blood through the veins toward the heart • 
but changes in the walls of the vessels from inflammation or injury, 
etc. , are not without influence. 

WOUNDS— RUPTURE. 

Wounds of the veins usually heal by a simple contraction and 
an adhesive inflammation of their walls ; sometimes by the forma- 
tion of a thrombus. Rupture of the veins may be produced by se- 
vere contusions and crushings of the body and by violent falls. 
Perforation of a vein may be produced by suppuration of the soft 
parts and the invasion of the walls of the vessel ; by the pressure of 
an aneurism or of a new growth ; by the thinning of the wall of 
the vein in phlebectasia. 

INFLAMMATION. 

Inflammation of the veins, phlebitis, may involve chiefly the ex- 
ternal layers— periphlebitis ; or the internal — endophlebitis ; or, 
as is very frequently the case, the entire wall may be affected. 
Phlebitis may be caused by the presence of a thrombus, by injuries, 
or by an infectious inflammation of the surrounding tissues. Throm- 
bosis of the vein, either primary or secondary, is a very constant 
accompaniment of phlebitis. 

Acute Phlebitis may commence as a suppurative periphlebitis or 
as a result of inflammatory processes about the vessel. The outer 
layers of the venous wall are congested, swollen, infiltrated with 
serum and pus. The inner coats may become infiltrated with pus; 
they may become necrotic and disintegrate. A thrombus is con- 
stantly formed under these conditions, which may for a time stop 
the circulation and keep the products of inflammation and degenera- 
tion from mixing with the blood ; but the thrombus itself is prone to 



THE VASCULAR SYSTEM. 



519 



disintegration, and thus the exudations and decomposing fragments 
of tissue may enter the circulation. 

On the other hand, owing to the presence of irritating or infec- 
tious material within the vein and the formation of a thrombus, the 
inflammatory process may be at the commencement an endophlebi- 
tis, bat usually, if the inflammation be at all severe, the entire wall 
of the vessel will eventually be involved. The pus cells in both 
cases doubtless come from emigration from the vasa vasorum. 
Acute phlebitis may terminate in the absorption of the thrombus and 
the return of the vein to its normal condition ; in the obliteration of 
the vein ; or portions of the thrombus may become detached and find 
their way as emboli into various parts of the body. The most im- 




Fig. 261. — Tuberculous Phlebitis. 
The section is from one of the pulmonary veins in a child dead of acute general miliary tuber- 
culosis. Specimen loaned by Dr. W. P. Northrup. 

portant results of phlebitis are usually those which depend upon the 
introduction into the blood of these emboli or of septic material (see 
Thrombosis and Embolism, page 72, and Pysemia). 1 

Chronic periphlebitis produces thickening, principally of the outer 
coats of the veins, but the inner coats may also be involved. The 
surrounding tissue may be also thickened and coalesce with the 
walls of the vein. There may or may not be thrombosis. 

Chronic endophlebitis is a not very common lesion, of the same 
general character as chronic endarteritis. More or less circum- 
scribed patches of new connective tissue are formed in the inner 
coats, which may undergo fatty or calcareous degeneration. 

Tuberculous Inflammation of the walls of the veins may occur 
as an extension of the process from without or from a lodgment of 
the tubercle bacilli in the blood current on the intima (Fig. 2G1). 



1 Consult Freudweiler, 
526, 1895. 



"Experimental Phlebitis," Yircb. Arch., Bel. cxli., p. 



520 THE VASCULAR SYSTEM. 

This is not infrequent in the pulmonary veins, and Weigert has called 
attention to the fact that in acute miliary tuberculosis the growth 
of tubercle tissue into the lumina of these veins from tubercular 
lymph nodes is of frequent occurrence and readily explains the 
topography and mode of occurrence of the general disease. The tu- 
bercle bacilli which are present in the tubercular tissue growing 
into the lumen of the veins find thus an easy distribution. 

Syphilitic Inflammation may involve the walls of the veins 
either as gummy tumors or as more diffuse thickenings. 

TUMORS. 

Primary tumors of the veins are rare. Small leiomyomata have 
been described in the saphenous and ulnar veins. A myosarcoma 
as large as a man's fist has been described, situated in the dilated 
vena cava inferior. The veins are not infrequently secondarily in- 
volved by sarcomata and carcinomata, and sometimes by chondro- 
mata. The thin walls of the veins offer comparatively little resist- 
ance to the encroachment of malignant tumors, which thus gain 
access to the circulation and may form metastases in various parts 
of the body. 

PARASITES. 

Echinococcus is sometimes found in the veins, having either de- 
veloped there or perforated from without. 

Two species of distoma {liver fluke) occur in man. D. hepati- 
cum occurs rarely in man, and, while usually found in the bile ducts, 
may occur in the vena cava. D. Jia3?natobium is very common in 
man in Egypt and in other parts of Africa, and usually occurs in the 
portal vein or its branches, and frequently in other veins. 

THE CAPILLAEIES. 

The walls of the capillaries are so thin and so intimately con- 
nected with the surrounding tissues that their lesions are studied 
most appropriately among the diseases of the several organs. Dila- 
tation of the new-formed capillaries in tumors, granulation tissue, 
etc., and fatty and hyalin degeneration of their walls, may be 
mentioned here as readily observed lesions occurring under a variety 
of conditions. The changes which we assume to occur in the walls 
of the smaller veins and capillaries in exudative inflammation, by 
reason of which fluids and blood cells pass through them, are not yet 
sufficiently understood to be described with definiteness. 

THE LYMPH VESSELS. 
The smaller lymph vessels can hardly be treated as independent 



THE VASCULAR SYSTEM. 521 

structures, since their walls are so closely joined with the tissues 
through which they pass ; the lymph radicles, indeed, being nothing 
more than the spaces in the connective tissue in which the variously 
shaped connective-tissue cells lie. In the larger lymph vessels we 
find a moderate number of more or less independent lesions. 

INFLAMMATION. 

Lymphangitis. 

Inflammation of the larger lymph vessels is usually secondary 
and connected with some wound or injury. Owing, it is believed, 
to the entrance into the lymph trunk of some septic material or bac- 
teria, the vessels, sometimes for a considerable distance away from 
the wound, become red, tender, and painful. Under these condi- 
tions the microscopical appearances which the vessels present vary. 
In some cases the redness disappears after death and we find no ap- 
preciable alteration. In other cases we find the walls of the lymph 
vessels more or less densely infiltrated with pus cells, and the lumen 
may contain variable quantities of pus and fibrin and desquamated 
endothelium. The tissue about the vessels may also be infiltrated 
with serum and pus. These lesions may undergo resolution and the 
vessel be restored to its normal condition ; or the vessel wall and sur- 
rounding tissue may die or become involved in abscess ; or new con- 
nective tissue may form in and about the vessel, sometimes with 
obliteration of its lumen. The lymph nodes may participate in the 
inflammatory process. 

Inflammation of the lymph vessels may occur as the result of dis- 
section and other wounds, and the bites of venomous reptiles. It 
may occur in the uterine lymphatics in the phlegmonous form of puer- 
peral fever, and under other conditions. 

Tuberculous Lymphangitis. — Tuberculous inflammation occurs 
both in large and small lymph vessels. Miliary tubercles and diffuse 
tubercle tissue may form in the walls and project into the lumen of 
the larger trunks ; or in the smaller vessels the new growth may en- 
tirely fill the lumen, and grow in this, with more or less involvement 
of the walls. This may occur independently, but it is most fre- 
quently seen in connection with tubercular inflammation of adjacent 
tissues. Thus from tubercular lymph nodes in the vicinity of the 
thoracic duct there may be a direct extension of the tubercular in- 
flammation, an involvement of the walls of the duct, and a growth 
of tubercle tissue into its lumen. Such growths in the thoracic duct 
have been shown by Weigert to be frequent in acute general miliary 
tuberculosis, and very satisfactorily explain the dissemination of the 
tubercle bacilli. In the vicinity of tubercular ulcers in the intestines, 



522 THE VASCULAR SYSTEM. 

furthermore, we often see the subserous lymph vessels, which pass 
from the vicinity of the ulcers, distended with the products of tuber- 
cular inflammation and looking like dense white knobbed cords. 

Syphilitic Inflammation of the lymph vessels not infrequently 
occurs in the vicinity of syphilitic ulcers in the primary stage. In 
later stages there may be thickening of the walls of the vessels and 
the development of gummy tumors in and about them. 

LYMPHANGIECTASIS. 

Dilatation of the lymph vessels occurs under a variety of condi- 
tions. It may be congenital, or it may be due to some hindrance to 
the flow of lymph onward — as by pressure from any cause, or from the 
occlusion of the vessels by inflammation — or it may be produced by 
unknown causes. If the dilated vessels form a circumscribed mass, 
this is often called a lymphangioma (Fig. 127). In certain forms of 
elephantiasis and in macroglossia the dilatation of the lymph ves- 
sels is an important factor. Its occurrence is not infrequent in the 
labia, prepuce, and scrotum. 

TUMORS. 

The relation of the endothelium of the lymph vessels and spaces 
to endotheliomata has been already mentioned in the section on 
Tumors. 

The dissemination of malignant tumors through the lymph chan- 
nels is of frequent occurrence, and is particularly marked in the case 
of carcinoma. In the vicinity of carcinomata the lymph vessels are 
not infrequently crowded with the tumor cells, forming white, irreg- 
ular cords ; or small masses of the tumor cells may be found in the 
lymph vessels, either near to or remote from the tumor. White, 
irregular networks are often formed in this way beneath the pleura 
in carcinoma of the lung (Fig. 131), or beneath the capsule of the 
liver. Transverse sections of lymph vessels thus distended show 
sometimes swelling and detachment of the endothelium and a crowd- 
ing of the lumen with tumor cells. Whether or not the endothelium 
participates in the new formation of the characteristic carcinomatous 
cells is not known. 

THE LYMPH NODES {Lymph Glands). 1 

It is well, in studying the lesions of the lymph nodes, to remember 
that they are structures so placed in the course of the lymph vessels 

1 What we call lymphatic tissue embraces not only the so-called lymph glands and 
the less complex but still well-defined structures found in the stomach, intestines, 
tonsils, and elsewhere, and called lymph follicles, but also the less well-defined, 



THE VASCULAR SYSTEM. 523 

that the lymph, in flowing toward the larger central trunks, passes 
through them, undergoing a sort of filtration as it percolates through 
the trabeculse of the lymph sinuses. If this simple fact be borne in 
mind the diseases of the lymph nodes, which are in the majority of 
cases secondary, are much more readily understood. Particles of 
pigment which in any way get into the lymph vessels are carried 
along until a lymph node is reached, and here they are, in part at 
least, deposited among the trabeculse of the sinuses, while the lymph 
passes on and out of the efferent vessels (Fig. 264). The same thing 
occurs when cells from malignant tumors, bacteria of various kinds, 
etc., gain access to the lymph vessels; and also, as there is good 
reason for believing, in the case of many poisonous materials which 
our present knowledge does not enable us to associate with bacteria. 
These various materials, filtered out of the lymph by the glands, may 
act in a variety of ways to produce lesions in them. 

INFLAMMATION. 

Acute Inflammation of the lymph nodes usually occurs in con- 
nection with some inflammatory process in the region from which its 
lymph is gathered. The nodes are in the majority of cases swollen, 
reddened, and softer than normal, and often the seat of smaller and 
larger hemorrhages. Sometimes one, sometimes several nodes of a 
cluster are affected. 

The microscopical examination shows the most prominent change 
to be a great increase in the number of cells in the f ollicles and cords, 
as well as in the lymph sinuses. These cells are, in part, small and 
spheroidal, and similar to those normally filling the meshes of the 
follicles ; in part large polyhedral or variously shaped cells with 
prominent nuclei ; the latter cells are most abundant in the lymph 
sinuses. In addition to this there is swelling of the endothelial cells 
of the reticulum of the sinuses (Fig. 262). The blood vessels may 
be distended with blood, or there may be blood, in greater or less 
quantity, free in the sinuses and follicles. The origin of the large 

irregular masses of tissue resembling that of lymph follicles, which, as Arnold has 
shown (Virchow's Archiv, Bd. lxxx., p. 315; Bd. lxxxii., p. 394; Bd. lxxxiii., p. 289; 
Bd. lxxxvii., p. 114), is widely disseminated in variable amounts in different parts of 
the body; in the lungs, beneath the pleura, and elsewhere ; in the liver, kidneys, etc. 
Although the exact nature of these more diffuse masses of lymphatic tissue is too 
little understood, as indeed is that of the lymph follicles and glands themselves, there 
is reason to believe that they are, analogous structures and prone to be affected by 
similar deleterious agencies. It seems better, in view of the fact that the so-called 
lymph glands are not glands at all, in the ordinary sense of the word, to call them 
lymph nodes, and the smaller masses of lymphatic tissue scattered through various 
parts of the body lymph nodules instead of " lymph follicles." 



524 



THE VASCULAR SYSTEM. 



number of new cells which may form in a very short time is not yet 
definitely known. They may be emigrated leucocytes or their de- 
rivatives ; they may be derivatives of the endothelium of the reti- 
culum ; or they may be in some cases, at least in part, cells which 
have been brought into the node, through the afferent trunks, from 
some external inflammatory focus. The capsule of the nodes, and 
not infrequently the connective tissue about them, may also be in- 
filtrated with round cells. 

Acute inflammation may terminate in resolution, the new cells 
disappearing either by fatty or other degeneration, or by being car- 
ried off in the lymph, and the node return to its normal condition. 




262.— Acute Inflammation of Lymph Node in Typhoid Fever. 
Showing a portion of one of the mesenteric nodes. A, capsule; B, perifollicular space or 
lymph sinus, containing in its meshes many large cells; C, portion of one of the follicles, with large 
and small cells in the meshes of its reticulum. 

This is the rule in the less intense forms of inflammation. On the 
other hand, the inflammatory process may become purulent and so 
intense as to lead to the formation of abscess, usually with a greater 
or less involvement of the tissue about the nodes. Fibrin and fluid 
exudate may be present in considerable quantity. There may be at 
first numerous small abscesses, which coalesce to form larger ones. 
These abscesses — buboes — may open externally or internally, or they 
may become dried and converted into cheesy masses which may 
calcify and, by a chronic inflammation in their periphery, become 



THE VASCULAR SYSTEM. 



525 



enclosed by dense connective tissue. Sometimes, instead of abscess 
being formed, the tissue of the inflamed nodes becomes necrotic and 
breaks down, inducing more or less severe inflammatory or necrotic 
changes in the tissues in their vicinity. Small necrotic foci alone 
may form. 

In still other cases acute inflammation of the lymph nodes 
passes into the chronic form. 

Moderate degrees of inflammation in the lymph nodes are very 
common in connection with various forms of inflammation in neigh- 
boring parts. Thus simple pharyngitis, gastro-enteritis, erysipelas, 
simple purulent inflammation, etc., are often associated with this 
lesion of the nodes. The lymph nodes of children are, as a rule, more 
easily affected by moderate inflammations in neighboring parts than 








W0mim 







'ft 



02sm&& 



Fig. 263.— Chronic Inflammation of Bronchial Lymph Node. 
Showing obliteration of the lymph sinuses and atrophy of the lymph follicles by the new-f ormect 
connective tissue. 

are those of adults. Purulent inflammation of the lymph nodes is 
most frequently associated with severer forms of inflammation of 
adjacent or related parts, especially those of an infectious character, 
syphilitic inflammation, poisoned wounds, pyaemia, etc. In a cer- 
tain number of cases we find bacteria in the inflamed lymph nodes, 
either singly or in zoogloea colonies, which have presumably some- 
thing to do with the lesion. 

In many cases the lesion of the lymph nodes appears to be in- 
duced, not by bacteria in the nodes themselves, but by poisons pro- 
duced elsewhere by the action of bacteria and brought to the nodes 
by the lymph. The swelling of the lymph nodes in typhoid fever 



520 



THE VASCULAR SYSTEM. 



and diphtheria is probably induced in this way. Necrotic urea in 
the lymph nodes may result from the presence of bacterial poison. 

Chronic Inflammation. — This is characterzed by the increase of 
the connective-tissue elements of the node, with a gradual and com- 
mensurate disappearance of the lymphoid cells. The reticulum of 
the follicles and sinuses becomes thickened and & ^ous, and in the 
trabeculse and capsule new connective tissue is form L , until, in ad- 
vanced cases, the entire node may be more or less completely con- 
verted into a mass of connective tissue. This condition is very fre- 
quently seen in the lower tracheal and in the bronchial nodes, 
apparently as a result of the lodgment in them of respired pigment 
particles ; but it may occur in any nodes, either as a result of re- 
peated moderate degrees of inflammation or from causes which we 




"ft 



Fig. 264,— Pigmentation of Bronchial Lymph Node. 
The pigment is largely in the lymph sinuses and enclosed in cells. A, capsule of node; B, 
lymph follicle; C, perifollicular lymph sinuses. 

do not know. In some cases the nodes are greatly enlarged and the 
new tissue contains many large cells, while in other cases the con- 
nective tissue is dense and contains but few cells (Fig. 263). 1 

Pigmentation. — The pigment which is very frequently found in 
lymph nodes may be derived from the hsemoglobin of the blood, 
either in the nodes themselves or in remote parts, or it may be 
formed of various materials introduced into the body from without, 
such as the pigments used in tattooing, respired dust particles of va- 



1 Consult Ribbert, " Ueber Regeneration und Entziindung der Lymphdruse*i, ' 
Ziegler's Beitrage zur path. Anat., Bd. vi., 1889, p. 187. 



THE VASCULAR SYSTEM. 527 

rious kinds — coal, stone, iron, etc. (Fig. 264). The pigment particles, 
which usually first lodge in the lymph sinuses, may collect here in 
large quantities, either in the reticulum or the cells lying in its 
meshes , they may penetrate the follicles and cords and find perma- 
nent lodgment there. They usually induce a greater or less degree 
of chronic inflammation, so that in extreme cases, such as are fre- 
quently seen in t ; bronchial lymph nodes, nothing is finally left of 
the node but a more or less deeply pigmented mass of dense connec- 
tive tissue. The function of the node is, of course, in this way par- 
tially or entirely destroyed. The pigment in these cases appears to 
reach the node, in part by being carried along free in the lymph cur- 
rent, in part by becoming enclosed in leucocytes and being trans- 
ported by them. Pigmentation of the nodes is most marked in 
those about the root of the lungs, which are frequently of a mottled 
gray or a black color, but it may occur in the mesenteric and other 
nodes. Under similar conditions the diffuse lymphatic structure in 
the lungs and liver may be similarly pigmented. 

Inflammation of the Lymph Nodes ivith Cheesy Degenera- 
tion. — This lesion of the lymph nodes, which is distinct from the 
above-mentioned comparatively infrequent cheesy degeneration of 
the contents of old abscesses, commences with changes similar to 
those above described in simple inflammation. The node in this con- 
dition is swollen and feels harder than normal ; on section it has 
a uniform reddish-gray color. Microscopical examination reveals a 
great increase in the number of parenchyma cells, some small and 
spheroidal, others large and polyhedral. Sometimes the larger cells 
are multinuclear, and not infrequently the reticular framework and 
the capsule are thickened. As the process advances the characteris- 
tic necrotic changes make their appearance. We may find at first a 
greater or less number of the cells converted into a strongly refrac- 
tile material, and the nuclei no longer capable of being stained. 
Then larger and smaller masses of cells undergo cheesy degenera- 
tion, with complete destruction of the blood vessels, reticulum, and 
the spheroidal and other cells, and their conversion into a granular 
material. A section through the node in this condition shows the 
cut surface mottled with irregular-shaped, larger and smaller opaque 
white patches, which indicate the areas of cheesy degeneration. 
These patches may increase in size and coalesce, so that a large part 
of, or even the entire gland may be converted into a more or less 
dense, cheesy mass which may be surrounded by the thickened 
capsule. 

In this condition they may remain for a long time, and not infre- 
quently, owing 'to the involvement of a series of associated nodes, 
either simultaneously or one after another, and the increase of con- 



528 THE VASCULAR SYSTEM. 

nective tissue about them, we find large, irregular nodular masses 
made up of a congeries of similarly affected nodes. 

On the other hand, the cheesy material may soften and break 
down, and, by the establishment of purulent and necrotic inflamma- 
tion about them, abscesses may form which may open externally. 
These abscesses may heal ; but usually the healing is difficult and 
slow, and long-continued suppurations, frequently with the develop : 
ment of fistulaa, are very common. Under these conditions the in- 
flammation may assume a tubercular character. Instead of soften- 
ing, the cheesy material in the glands may become dry and hard and 
undergo calcification. 

Cheesy inflammation of the lymph nodes is most common in the 
cervical, bronchial, and mesenteric groups, but may occur anywhere. 
It is most apt to occur in badly nourished young persons, who, in 
addition to the lesion of the lymph nodes, are very liable to suffer 
from chronic inflammations of the mucous membranes, skin, perios- 
teum, joints, and the subcutaneous and other connective tissues. 
This general condition is known as scrofula, and the lesion of the 
nodes is sometimes called scrofulous inflammation. It is not in- 
frequently associated with tuberculous inflammation of the nodes, 
either as an independent lesion or as a part of a general tuberculosis, 
and by some writers tuberculous and scrofulous inflammation of the 
lymph nodes are considered to be identical. In a considerable pro- 
portion of cases, however, of so-called scrofulous inflammation of the 
lymph nodes, there is no formation of tubercle tissue and we find no 
tubercle bacilli, so that we must consider this class of cases as sim- 
ply inflammatory, with a tendency to cheesy degeneration. 

Tuberculous Inflammation may occur in connection with simple 
inflammatory changes in the lymph nodes, or with the form of in- 
flammation which tends to cheesy degeneration. It may be local, 
confined to the nodes, or it may occur in connection with general 
acute miliary tuberculosis or with tuberculous inflammation of single 
organs. It may occur in single nodes, or in several nodes of the same 
group, or in groups situated in different parts of the body. In its 
simple and acute form there may be no evident change to the naked 
eye in the appearance of the nodes, or they may be besprinkled with 
small, grayish-white, translucent spots. Under these conditions the 
nodes may be reddened and soft, or swollen and denser than normal. 
In more advanced forms of the lesion the tubercles coalesce and un- 
dergo a greater or less degree of cheesy degeneration. Under these 
conditions the cheesy areas are evident to the naked eye as more or 
less sharply circumscribed, opaque, whitish areas, frequently sur- 
rounded by an irregular, more translucent, grayish zone of tubercle 
tissue which merges insensibly into the adjacent tissue. The entire 



THE VASCULAR SYSTEM. 529 

node may become involved, and more or less completely converted 
into a cheesy mass, in the periphery of which a zone of tubercle tis- 
sue may or may not be evident. 

Microscopically the small nodules or miliary tubercles are seen to 
consist of more or less circumscribed collections of small spheroidal, 
or more frequently larger polyhedral cells, with or without well-de- 
fined giant cells. They usually commence to form in the follicles 
and lymph cords of the nodes, and from these may spread and involve 
the entire surrounding tissue. The cheesy degeneration, which here 
as elsewhere is apt first to involve the central portions of the tuber- 
cles, presents the usual appearances. Tubercle bacilli may be found 
in the edges of the cheesy areas or in the tubercle tissue about them. 

Simple inflammatory changes regularly occur in the periphery of 
the tubercles. There is an increase of cells in the lymph sinuses and 
follicles, and a more or less marked swelling, and apparently a pro- 
liferation of the cells of the reticular tissue of the node. In cases in 
which the process is chronic there is often marked increase of the 
connective tissue of the nodes, the reticular tissue becomes dense 
and fibrous, and the trabeculoe and capsule are thickened. The 
tubercles themselves, instead of undergoing cheesy degeneration, 
may become fibrous or be converted into a hyalin material. 

The cheesy material may dry and shrink, and become enclosed 
by a capsule of dense connective tissue and become calcified ; or it 
may soften, and thus cavities be formed in the glands, filled with 
grumous material ; or inflammatory changes may be induced in the 
vicinity of the nodes, leading to abscesses. On the other hand, hy- 
perplastic inflammation in the periphery of the affected nodes may 
result In their becoming bound together into a dense nodular mass. 

When cheesy degeneration has occurred, to the naked eye tuber- 
culous lymph nodes may not be distinguishable from those in scrofu- 
lous inflammation, but in some cases the nodular character of the 
new tissue around the cheesy centres is evident. The process is 
usually a slow and chronic one, except when occurring in connection 
with acute miliary tuberculosis in other parts of the body. It may 
occur in any of the nodes, but is most frequent in those of the bron- 
chial, mesenteric, and cervical regions. ] 

Syphilitic Inflammation. — The lesions of the lymph nodes 
which occur in connection with syphilitic poisoning vary greatly, 
depending upon the stage of the disease. In the primary stage the 
lymph nodes in the region of the seat of infection are apt to pre- 
sent the lesions of an ordinary acute inflammation, with a tendency 
to the assumption of the purulent form. 



1 For a consideration of the significance of tuberculous bronchial lymph nodes 
in children, consult Mrthrup, New York Medical Journal, February 21st, 1891. 
43 



530 THE VASCULAR SYSTEM. 

In the secondary stage of the disease the nodes of other regions, 
neck, elbow, axilla, etc., are frequently swollen and hard. On 
microscopical examination there may be an increase of connective 
tissue in the capsule and trabecule, but the chief change is in the 
accumulation in the follicles and lymph sinuses of larger and smaller 
spheroidal and polyhedral cells. The reticular tissue may be thick- 
ened and the walls of the blood vessels infiltrated with cells. In 
this condition the nodes may remain for a long time, not tending to 
form abscess ; or they may undergo resolution through degenera- 
tion and absorption of the cells. 

In the tertiary stage of the disease the nodes may be the seat of 
chronic inflammation characterized by the formation of gummy 
tumors. Under these conditions they may form large, firm nodular 
masses by the growing together by new connective tissue of several 
altered nodes. The gross and microscopical characters of gummata 
of the lymph nodes are, in the main, similar to those in other parts 
of the body. 

There are important changes in the lymph nodes which occur as 
local manifestations of general diseases, such as typhoid fever, 
leprosy, etc., which will be considered under the headings of these 
diseases. 

Degenerative changes in the lymph nodes, with the exception 
of those above described, are not of great frequency or significance. 

Atrophy is a very regular occurrence in old age. In this con- 
dition the nodes are small, hard, and, unless pigmented, white. 
Microscopical examination shows a marked diminution in the num- 
ber of parenchyma cells, while the reticulum and the capsule and 
trabeculse may be thickened. There may be an accumulation of 
fat around the node in connection with senile atrophy. 

It should be remembered, in this connection, that the lymph 
nodes, as well as the lymphatic tissue in general, in children are 
more voluminous and contain a greater number of parenchyma cells 
than in adults. 

Amyloid degeneration of the blood vessels and reticulum of the 
lymph nodes occurs under the conditions which favor this change in 
general. It may occur in connection with amyloid degeneration of 
other parts of the body, or by itself. It may occur in nodes other- 
wise normal, or in those which are the seat of other lesions — thus in 
simple chronic or tubercular inflammation. It is frequently found 
in the mesenteric lymph nodes, in connection with waxy degenera- 
tion of the intestinal mucous membrane. 

Hyalin degeneration of the external layers of the smaller 
arteries and the capillaries of the lymph nodes, and also of the 
parenchyma cells, occurs occasionally in old age or in connection 



THE VASCULAR SYSTEM. 531 

with wasting diseases. The vessels and cells are swollen and con- 
verted into a translucent, strongly ref ractile substance resembling 
amyloid optically, but not responding to its micro-chemical tests. 
By the accumulation of this material the uninvolved parenchyma of 
the nodes may be compressed and atrophied. 

hyperplasia of the lymph nodes (Lymphoma). 

In addition to the considerable enlargements of the lymph nodes 
in inflammation which have been described above, they become en- 
larged under a variety of conditions which we do not understand. 
This lack of knowledge of the etiology, together with our ignorance 
of the function of the lymph nodes, and the morphological similarity, 
or even identity, which these enlarged nodes present, render it very 
difficult to decide upon the exact nature of the change, and in many 
cases to distinguish one form from another. 

In the first place, there is a class of cases in which, sometimes 
slowly, sometimes with great rapidity, the lymph nodes of certain 
regions, especially the abdominal, axillary, cervical, and inguinal, 
enlarge not infrequently to an enormous extent. They may be 
either hard or soft, even almost fluctuating ; the individual nodes 
may be distinct or merged into one another. Sometimes the nodes 
in nearly all parts of the body are affected. Microscopically we find 
that the enlargement is due, in the soft varieties, to an enormous 
increase of small spheroidal and polyhedral cells and a growth of 
the reticular tissue. It is a new formation of lymphatic tissue, but 
the normal relations of follicles, cords, and lymph sinuses are not pre- 
served. In the harder varieties there is a thickening of the reticular 
tissue in addition to an increase of cells. In very rare cases portions 
of the nodes may become cheesy. Sometimes larger and smaller 
haemorrhages occur in the nodes, especially in the softer forms. In 
addition to these changes in the lymph nodes there is, in a consider- 
able proportion of cases, a new formation of lymphatic tissue in 
greater or less quantity in other parts of the body, in the spleen, in 
the gastro-intestinal canal, in the marrow of bones, in the liver, kid- 
neys, etc., and the number of leucocytes in the blood and in other 
parts, of the body is increased. This general condition is known as 
leukaemia and will be considered under the general diseases. The 
enlarged lymph nodes in this disease may be called, for convenience, 
leukaimic lymphomata. 

In the second place, there is a form of disease in many respects, 
particularly in the lesion of the lymph nodes, resembling leukaemia. 
There is, however, usually a less prominent involvement of the spleen 
and other lymphatic structures, and, what is more striking, no 
increase in the number of leucocytes in the blood. This is called Hodg- 



532 THE VASCULAR SYSTEM. 

kin's disease, or pseudo-leiikcemia, and the enlarged lymph nodes 
may in this case be called psendo-leukoemic lymphomata. The lesions 
of the lymph nodes are similar in both diseases, and it is convenient 
to assign different names to them simply because, for reasons which 
we do not at all understand, they seem to arise under different condi- 
tions and to be associated with a constant difference in the character 
of the blood (see page 794) . 

TUMORS. 

Sarcomata occur in the lymph nodes as primary and second- 
ary tumors, and these may be of various forms : spindle-celled, 
large and small round-celled, and angio-sarcomata. It is not easy 
in many cases to distinguish morphologically between the small 
round-celled sarcomata and the above-described lymphomata. Fi- 
bromata, myxomata, and chondromata occur in the lymph nodes, 
but are rare. Endotheliomata are described, but are not common. 
Secondary carcinomata are of frequent occurrence, the form of the 
cells and the nature of their growth depending upon the seat and 
character of the primary tumors. 

PARASITES. 

Aside from various Torms of bacteria which are not infrequently 
found in the lymph nodes — thus in diphtheria, splenic fever, typhoid 
fever, tuberculosis, etc. — filaria, trichinae, and pentastomum have, 
been described. 



THE ALIMENTARY CANAL. 



THE MOUTH. 



MALFORMATIONS. 



Malformations of the lip and cheeks are usually associated with 
defective formation of the bones of the mouth. The entire process is 
generally due to an arrest of development. 

1. The lower jaw is absent ; the upper jaw and hard palate small 
and imperfectly formed ; the temporal bones nearly touch in the 
median line. The lower part of the face is, therefore, wanting ; the 
mouth is absent, or small and closed posteriorly; the tongue is absent. 
Such a malformation is rare ; the foetus is not viable. 

2. The face remains in its early foetal condition of a large cleft ; 
the mouth and nose form one cavity ; the orbits may be united in the 
same cavity. The foetus is not viable. 

3. There is a cleft in the upper lip, upper jaw, and hard palate. 
The cleft corresponds to the point of junction of the processes of the 
superior maxilla with the intermaxillary bone. There may be one 
cleft or two, one on either side of the intermaxillary bone. The cleft 
involves the lip alone, or the lip and superior maxilla, or the lip, 
maxilla, and palate. There may be a single or a double cleft in the 
palate, and the cleft may involve either the hard or soft palate, or 
both. If there are two clefts of the lip and maxilla the portion of lip 
and bone between them may be small, or entirely absent so as to 
leave a large open space. The soft palate may be entirely absent. 
This is a common malformation and does not endanger life. 

4. Rarely we find a cleft involving the middle of the lower lip, 
and sometimes extending into the inferior maxilla. 

5. Either the inferior, the superior, or both maxillary bones may 
be abnormally small. 

6. The edges of the lips may be partly or completely joined to- 
gether. The opening of the mouth may be only a round hole. 

7. The lips may be absent or imperfectly developed. 

8. The corners of the mouth may be prolonged by clefts in the 
cheeks nearlv' to the ears. 



534 THE ALIMENTARY CANAL. 

HYPERTROPHY. 

The skin of the cheeks and lips may be hypertrophied in connec- 
tion with elephantiasis of the face. 

There may be a thickening of the lips alone, so that they appear 
double. This thickening may be due to an increase of all the ana- 
tomical elements of the lips ; or there may be an increase and dilata- 
tion of the lymphatic vessels, giving to the growth a soft, cedematous 
character. 

INFLAMMATION. 

Catarrhal Stomatitis is found most frequently in children. It 
is produced by a great variety of local and constitutional causes. Of 
the conditions which are seen during life, the congestion, increased 
production of mucus, and swelling of the mucous membrane, but 
little remains after death. 

During life the congestion and swelling of the mucous membrane 
are well marked. There are often white patches, produced by the 
death of the superficial epithelial cells. There may be an increased 
production of mucus, which runs constantly from the mouth, or, in- 
stead of this, the entire mucous membrane is unnaturally dry. 

The only structural changes which can be demonstrated are the 
degenerative changes of the epithelial cells and the production of pus 
cells, which infiltrate to a moderate degree the stroma of the mucous 
membrane and appear upon its surface. Small clear vesicles may 
form beneath the epithelium from the collection of serous exudate. 

Croupous Stomatitis is produced by local irritants, by extension 
of the same form of inflammation from the pharynx, and it occurs 
with the exanthematous fevers and with diphtheria. 

Portions of the mucous membrane are swollen and congested, and 
covered with a false membrane. This false membrane is composed 
of a thickened layer of epithelium in the condition of coagulation 
necrosis, and of fibrin and pus in variable relative quantity. The 
stroma of the mucous membrane may be infiltrated with pus and 
fibrin, and portions of it may become necrotic. 

stomatitis ulcerosa 1 (Stomacace ; St o mat it e Ulcero-mem- 

braneuse). 

This form of stomatitis occurs in children between the ages of 
four and eight years, and in adults between the ages of eighteen and 
twenty-five years. It is apt to occur in localized epidemics, in hos- 
pitals and asylums, and among soldiers and sailors. Some of the 
forms of mercurial stomatitis seem to be identical with this form of 
inflammation. 

1 Bergeron, " Stomatite ulcerosa," Union Medicale, 1859. Bohn, " Mundkrank- 
heiten der Kinder," 1880. 



THE ALIMENTARY CANAL. 535 

The inflammation begins at the margin of the gums of the lower 
jaw. The gums are swollen and coated with a grayish, soft matter 
composed of bacteria and detritus. Then follows destruction of tis- 
sue ; the gums are destroyed around the teeth, and these fall out ; 
the inflammation extends to the lips, cheeks, and tongue. The 
ulcers are coated with a thick, soft, gray membrane. The surround- 
ing soft parts are swollen, and there may be necrosis of the jaws. * 

Syphilitic Stomatitis. — As a result of syphilis there may be pro- 
duced either the so-called mucous patches or gummy tumors. In 
the mucous patches we find at first the epithelial layer thickened 
and the papillae of the stroma swollen and infiltrated with cells. 
This may be followed by desquamation of the epithelium and ulce- 
ration of the stroma. 

The deeper gummy tumors may also soften and form ragged 
ulcers of some size. 

Tubercular Stomatitis commences with the formation of miliary 
tubercles or of larger tubercular masses in the stroma of the mucous 
membrane. These masses soon degenerate, soften, and form ragged 
ulcers resembling very closely syphilitic ulcers. 

GANGRENE. 

Gangrene of the lips and cheeks, or noma, is most frequent in ca- 
chectic children as a consequence of the abuse of mercury. Much 
more rarely it occurs in adults after typhus and other exhausting 
diseases. The disease begins in the mucous membrane of the cheeks 
near one of the corners of the mouth. The mucous membrane be- 
comes black and gangrenous ; the gangrene extends rapidly through 
the entire thickness of the cheek and produces perforation ; it ex- 
tends laterally in all directions. 

TUMORS. 

Adenomata are formed in the mucous membrane covering the 
mouth, lips, and soft palate. The tumors are rounded, usually small, 
sometimes as large as a hen ? s egg. They may be situated in the 
thickness of the mucous membrane, or project in a polypoid form. 
They are formed by an hypertrophy of the normal mucous glands. 
The glandular acini are increased in number and size, the epithelial 
cells are increased in number and may undergo colloid degeneration. 

Papillomata occur most frequently at the edges of the lips, but 
are also found on the gums, the floor of the mouth, and the cheeks. 

1 R. Volkmann, Virch. Arch., Bd. l.,p. 143, describes five cases of inflammation 
of the mucous glands of the lower lip. The lip was swollen and hard, the mucous 
glands and their ducts were dilated. 



536 THE ALIMENTARY CANAL. 

They are formed of hypertrophied papillae, covered with thickened 
epidermis. They very often alcerate. 

Carcinomata are of frequent occurrence. They may be found 
at any part of the mucous membrane of the mouth, but as a rule be- 
gin in the edge of the lower lip. 

They may orginate in an ulcerating papilloma, or as a flat, super- 
ficial growth from the deeper layers of the epithelium, or as deep 
nodules starting in the mucous glands. They are composed of large 
masses of epithelial cells, closely packed together, often forming 
nests, and arranged in anastomosing tubular masses. The stroma 
surrounding these masses is infiltrated with cells. In a few cases 
the infiltration of the stroma with small round cells may be very 
marked, so marked that the epithelial growth may be obscured. 
The new growth increases in size, ulcerates, infiltrates the adjacent 
tissues, and may give rise to metastatic tumors. 

Angiomata are found in the lips. They may be congenital or 
developed after birth. 

Fibromata, lipomata, and enchondromata have been seen in a 
few cases in the lips. When they appear in the mouth they usually 
grow from the bones. 

THE TONGUE. 
MALFORMATIONS. 

Absence of the tongue is found in connection with the extreme 
defects of development of the face already mentioned. 

The anterior portion of the tongue may be absent while its base 
remains. The lower jaw is then small. 

The tongue may be partly or completely adherent to the floor of 
the mouth. The frenulum may be abnormally short, or may extend 
to the tip of the tongue. In rare cases the sides of the tongue are 
adherent, or its upper surface may be adherent to the roof of the 
mouth. 

HYPERTROPHY. 

Macroglossia, or hypertrophy of the tongue, is almost always a 
congenital lesion, and is especially common in cretins. The tongue 
is so large that the cavity of the mouth cannot contain it ; it is pro- 
truded through the lips and displaces the jaws. The lips may also 
be hypertrophied in the same way. 

There is an hypertrophy of all the anatomical elements which 
make up the tongue, and in addition to this there may be a dilatation 
of the lymphatic vessels. 



THE ALIMENTARY CANAL. 537 



INFLAMMATION. 



Inflammations of the tongue may be associated with similar 
changes in the mouth, or may occur by themselves. 

Superficial Glossitis. — Inflammation involving only the mucous 
membrane of the tongue may occur as an acute or chronic process. 

The acute forms present no marked lesions. 

The chronic forms result in an increased production of epithelium 
and an hypertrophy of the papillae of the tongue. 

A moderate development of such an inflammation is not infre- 
quently associated with derangements of the stomach. The tongue 
is large, its surface is irregular from the hypertrophy of the papillae. 
There may be no change in the epithelium, and then the surface of 
the tongue is clean and red ; or the epithelium is increased and the 
tongue is covered with a white fur. 

More severe forms of the disease also occur, especially with 
syphilis. The hypertrophied papillae and increased epithelium then 
alter very decidedly the appearance of the tongue. 

Parenchymatous Glossitis may be produced by mercurial poison- 
ing, by injury, or by unknown causes. The tongue is swollen, the 
muscular and connective portions are congested and infiltrated with 
serum and pus. The inflammation may stop at this point or it may 
go on to the formation of an abscess. 

Syphilitic Glossitis. — In persons suffering from constitutional 
syphilis there may be mucous patches on the surface of the tongue ; 
or gummy tumors in its stroma, which often soften and form deep 
ulcers; or a diffuse, chronic inflammation of the surface of the tongue, 
with hypertrophy of the papillae. 

Tubercular Glossitis. — There may be a tubercular inflammation 
of the connective tissue of the tongue just beneath the epithelial 
layer, resulting in the formation of tubercle granula and granulation 
tissue. In this way tumors of some little size are formed, which 
may remain unchanged for some time, or may degenerate, soften, 
and form ulcers. 

TUMORS. 

Cysts. — The most common forms of cysts are the sacs beneath or 
partly in the substance of the tongue (ranula). They are formed by 
dilatation of the ducts of the submaxillary and sublingual glands, or 
make their appearance in the connective tissue beneath and in the 
tongue. 

Angioma. — Cavernous vascular tumors are found in the sub- 
stance of the tongue and projecting from its surface. 

Lipoma and fibroma are rare. They form nodules in the sub- 
stance of the tongue or project in a polypoid form. Composite 



538 THE ALIMENTARY CANAL. 

tumors, composed largely of fat, are found on the tongue as a con- 
genital condition. 

Lupus occurs in the form of nodules and ulcers at the base of the 
tongue. 

Sarcomata are not common in this situation, but they may occur 
both in children and in adults. 

Carcinoma. — This form of new growth may begin in the tongue 
or may extend to it from the adjacent tissues. The growth is com- 
posed of large, flat epithelial cells packed closely together in anas- 
tomosing tubular spaces and surrounded by a connective-tissue 
stroma. 

Amyloid tumors of the tongue have been several times reported. 
Micro-organisms of various forms; bacteria, moulds, and yeasts, are 
always present in the mouth, often in enormous numbers. They are 
for the most part not of significance save for the putrefactive pro- 
cesses which they initiate and maintain in mouths not properly 
cleansed. On the other hand, Staphylococcus and Streptococcus pyo- 
genes and the pneumococcus are of frequent occurrence in the mouths 
especially of those who live in towns and crowded dwellings. 

The tubercle bacillus may be present in the mouth as well as in 
the nose of those who care for uncleanly consumptives. The fungus 
of aphthae (soor), and leptothrix, which under usual conditions are 
not harmful, may incite serious local disease. 

The so-called Mycosis pharyngis is apparently due to the growth 
in susceptible persons of a form of leptothrix not yet thoroughly 
studied, on account of the technical difficulties in the way of its arti- 
ficial cultivation l (see page 284) . 

THE PHARYNX AND THE (ESOPHAGUS. 
MALFORMATIONS. 

When, as not infrequently occurs, the embryonal gill clefts do not 
properly close, fistulae may remain. These may in rare cases be 
complete, so that an opening exists from the pharynx, larynx, or 
trachea to the side of the neck. More frequently, however, these 
fistulae are incomplete and shallow, and open either inward into one of 
the above-named organs or outward on to the neck. Small portions 
of the gill clefts may persist without external openings, and from 
these subcutaneous cysts of the neck are often developed. Or a por- 

1 For the results of systematic studies on the bacteria of the mouth consult the 
works of Miller and of David. For bibliography and studies on micro-organism asso- 
ciated with acute angina see Stoos, Mitth. a. d.klin. med. Inst, der Schweiz, 3. Reihe, 
Heft 1, 1896, and for membranous rhinitis, Abbott, Medical News, May 13th, 1893; 
for ozoena, Abel, Zeits. f. Hygiene und Infectkr., Bd. xxi., p 89. 



THE ALIMENTARY CANAL. 



539 



tion of the cleft may be cut off, forming a cyst, while the fistula per- 
sists with its external opening. 

The walls of these fistulse and cysts may be covered with mucous 
membrane having cylindrical or flattened or ciliated surface cells. 




Fig. 265.— Section op the Wall op a Cyst of the Neck. 
Formed from imperfect closure of embryonal gill clef t— diffuse lymphatic tissue. 




Fig. 266.— Section of the Wall of a Cyst of the Neck. 
Formed from imperfect closure of embryonal gill clef t— nodules of lymphatic tissue. 

Or, when formed from the outer gill clefts, they may be lined with 
skin. 1 

1 Schmidt, Virch. Arch., Bd. cxliii., p. 369. Literature of amyloid tumors in 
general. 



MO 



THE ALIMENTARY CANAL. 



Not infrequently the walls of these cysts and fistulae are embedded 
in lymphatic tissue, which may be diffuse or gathered in nodular form 
(see Figs. 265 and 266). 

The oesophagus may be entirely absent, or its lower portion may 
be present and joined to the pharynx by a solid cord; or the pharynx, 
or the lower part of the oesophagus, may be continuous with the 
trachea ; or the entire oesophagus may be represented by a solid cord. 

Diverticula of the pharynx, dilatations of the oesophagus, and di- 
vision of the middle portion of the oesophagus into two branches have 
all been observed. 



INFLAMMATION. 

Catarrhal and Croupous Pharyngitis are usually associated 
with the same forms of inflammation in the mouth and have the 
same characters. 

In catarrhal inflammation involving the tonsils and those portions 
of the pharynx richly r supplied with the so-called submucous adenoid 
tissue, 1 leucocytes may penetrate in considerable numbers the peculiar 
thin epithelium. 2 These may, on exposed surfaces, form a part of 
the exudate and be removed; or in the crypts of the tonsils they may, 
with epithelium and various forms of bacteria, form those whitish 
plugs characteristic of follicular tonsillitis. 

In chronic inflammation of the tonsils and pharynx there may 
be a large and permanent hyperplasia of the adenoid tissue, with more 
or less dense fibrous tissue, leading to enlargement of the tonsils and 
to diffuse or circumscribed nodular or pedunculated masses of vas- 
cular new tissue in the vault or elsewhere in the pharynx. The ton- 
sils, on the other hand, may atrophy. 

Submucous Pharyngitis may occur with inflammations of the 
mucous membrane, with caries of the cervical vertebrae, with inflam- 
mation of the cervical and parotid glands, with periostitis of the 
cranial bones, or may be idiopathic. It may result in swelling and 
oedema, in induration, or in suppuration. It is most important 
when it affects the posterior wall of the pharynx and forms retro- 
pharyngeal abscesses. Such abscesses may cause death by suffo- 
cation. 

Catarrhal Oesophagitis may be either acute or chronic. The 
chronic form may produce ulceration, or relaxation and dilatation of 
the walls, or hypertrophy of the muscular coat. 

1 Consult DobrowoMi, "Lymph Nodules of the Larynx, (Esophagus, etc.," 
Ziegler's Beitrage z. path. Anat., Bd. xvi. , p. 43. 

*8eeH9denpyl, '• Anatomy and Physiology of the Faucial Tonsils," Am. Jour. 
Med. Sciences, March, 1891. 



THE ALIMENTARY CANAL. 541 

Croupous Oesophagitis is found with croup of the pharynx, and 
after the exanthemata and other severe diseases. 

Irritating and caustic acids and alkalies destroy larger or smaller 
portions of the mucous membrane. The necrosed portions are of a 
black or whitish color, surrounded by a zone of intense congestion. 
If the patient recover the patches of membrane which have been 
destroyed slough, fall off, and leave a granulating surface. In this 
way dangerous stenosis of the oesophagus may be produced. 

Foreign bodies which are swallowed and become fixed in the oeso- 
phagus cause inflammation of the mucous membrane and of the ad- 
joining soft parts. The inflammation may go on to produce ab- 
scesses around the oesophagus, or to destroy the wall of the canal, 
and the foreign body finds its way into the trachea, aorta, or peri- 
cardium. 

Inflammation of the submucous tissue of the oesophagus, apart 
from the cases just mentioned, is not common. It may cause the 
formation of abscesses, or of fibrous tissue, which may produce 
stenosis. 

ULCERATION. 

Ulceration of the pharynx occurs in rare cases as the result of 
catarrhal inflammation. More frequently it is produced by syphilis, 
either in the form of superficial ulcers or of deep and extensive de- 
structions of tissue from the softening of gummy tumors. 

Lupus also sometimes attacks the upper part of the pharynx 
and produces extensive ulceration. Ulceration of the oesophagus is 
not common, but a few cases of simple perforating ulcers have been 
described. l 

Foreign bodies in the oesophagus may perforate its wall, as al- 
ready mentioned. Perforation of the oesophagus from without may 
be produced by inflamed bronchial glands, by cavities and gangrene 
of the lungs, by abscesses in the mediastinum, by abscesses ac- 
companying caries of the vertebrae, and by aneurisms of the aorta. 
Cases have been described of rupture of the wall of the oesophagus 
by violent coughing and vomiting, but it seems probable that there 
was really some previous disease to account for the rupture. 



Simple cylindrical dilatation of the oesophagus is usually the re- 
sult of long- continued stenosis of the oesophagus or of the cardiac 
end of the stomach, although not nearly all the stenoses are fol- 
lowed by dilatation. These dilatations are formed at first immedi- 

1 Oraefe u. Watfher, Jour, far Chir. uad Augenheilk. , Bd. xix. Med. Chir. 
Trans., vol. xxxvi. Rokitansky, "Path. Anat." 

2 Ziemsxen, "Cyclopaedia of Medicine," viii., p. 47. 



542 THE ALIMENTARY CANAL. 

ately above the stenosis and then extend upward. Only in rare cases 
does the dilatation involve the whole length of the tube. The entire 
wall of the dilated portion of the oesophagus is thickened, and there 
may be polypoid growths from the mucous membrane. 

In rare cases there is cylindrical dilatation of part or of the whole 
of the oesophagus without a stenosis or any discoverable cause. In 
these cases the dilatation is usually greatest near the middle of the 
oesophagus and diminishes upward and downward, so that the oeso- 
phagus has a fusiform shape. The dilatation may reach a very con- 
siderable degree, the walls of the oesophagus are thickened, its 
mucous membrane may be covered with papillary outgrowths or 
ulcerated. 

The Sacculated Dilatations of the oesophagus are of two kinds : 
those due to pressure, and those due to traction. 

The dilatations due to pressure are situated in the posterior wall 
of the pharynx, just at its junction with the oesophagus. The 
smaller sacs are from the size of a pea to that of a hazelnut ; the 
larger sacs may reach an enormous size and hang down between the 
oesophagus and the vertebral column, the opening into the oesopha- 
gus remaining comparatively small. It is supposed that a limited 
area of the wall of the oesophagus loses its power of resistance against 
the pressure exercised upon it in each act of swallowing ; it then is 
forced outward by the pressure, and so there is formed first a protru- 
sion and then a sac. When a sac is formed the food enters it, accu- 
mulates there, and so the sac becomes larger and larger. 

The dilatations due to traction are situated on the anterior wall of 
the oesophagus, at a point nearly corresponding to the bifurcation of 
the trachea. They are of funnel shape, with the small end outward. 
Their length varies from two to twelve millimetres ; the width of the 
opening into the oesophagus is from six to eight millimetres. 

These dilatations are due to inflammation of the parts adjoining 
the oesophagus, especially of the bronchial glands, followed by ad- 
hesions to some part of the anterior wall of the oesophagus. These 
adhesions then contract and draw the wall of the oesophagus out- 
ward, and in this way the dilatations are formed. 

At a later time these sacs may perforate into the bronchi, the 
lungs, the pleural cavity, the pericardium., the aorta or pulmonary 
artery. 

STENOSIS. 

Congenital Stenosis. — Besides the defects of development of the 
oesophagus which are incompatible with life, there may be a congen- 
ital stenosis of some part of it which causes difficulty in swallowing, 
but yet does not destroy life. 

Stenosis by Compression is not uncommon. Tumors of the 



THE ALIMENTARY CANAL. 543 

neck and mediastinum, and aneurisms of the aorta are the usual 
causes. 

Stenosis by Obstruction.— foreign bodies may be lodged in the 
oesophagus. Tumors may hang down from the pharynx into the 
oesophagus, or may be situated in the wall of the oesophagus. In- 
flammation of the oesophagus, due to the ingestion of irritating poi- 
sons, produces cicatricial stenoses. A few cases of stenosis due to 
syphilitic inflammation have been reported. 

TUMORS. 

The veins of the oesophagus may be enormously dilated. They 
may rupture and so give rise to haemorrhage.' 

Cysts. — Small retention cysts of the follicles of the mucous mem- 
brane are sometimes found. Larger cysts of the oesophagus lined 
with ciliated epithelium have been described. 2 

Papillomata of small size may be found in considerable numbers 
throughout the entire length of the oesophagus, or may occur singly. 
Large papillary tumors are more rare. 

Fibromata grow from the periosteum of the bones at the base of 
the skull, and project into the cavity of the pharynx and posterior 
nares in the form of large polypoid tumors. Small fibrous tumors 
are formed in the submucous connective tissue of the oesophagus. 
Tumors, which attain a very large size, originate in the submucous 
connective tissue on the anterior wall of the lower part of the pharynx, 
and as they grow hang down into the oesophagus. Soft polypoid 
tumors consisting largely of loose succulent connective tissue and 
lymphatic tissue are often called ''adenoid polyps" (see Fig. 267). 
Hairy polyps of the pharynx have been described by Arnold 3 and 
others. The occurrence of cartilage and bone in the tonsil has been 
described by Stoeltzner. 4 

Lipomata of small size are sometimes found in the walls of the 
oesophagus. 

Myomata composed of smooth muscle may grow in the muscular 
coat of the oesophagus and attain a considerable size. 5 

Adenoma. — A polypoid adenoma composed of tubules lined with 
cylindrical epithelium, and growing from the anterior wall of the 
oesophagus, has been described by Weigert. 6 

l Bristoice, Trans. London Path. Soc. , 1856. 
*Zahn, Yirch. Arch., Bd. cxliii., p. 171. 
3 Arnold, Yirch. Arch., Bd. cxi., p. 176. Bibliography. 
4 Stoeltzner, Yirch. Arch., Bd. cxli., p. 446. 

5 Yirch. Arch., Bd. xliii., p. 137. Med. Times and Gazette, November 28th, 
1874. Glasgow Med. Journal, February, 1873. 
6 Yirch Arch., Bd. lxvii., p. 516. 



5U 



THE ALIMENTARY CANAL. 



I (Delafield) have seen one tumor, the size of a chestnut, growing 
in the soft palate, which was composed of a stroma of connective and 
mucous tissue in which were irregular, anastomosing tubules filled 
with small, polygonal, nucleated cells. It should be called an ade- 
noma or a carcinoma. 

Another composite tumor grew from the mucous membrane of the 
pharynx behind the left tonsil. It filled the pharynx below the level 




Fig. 267.— Adenoid Polyp of Pharynx. 



of the palate. It had the gross appearance of a myxo-sarcoma, the 
central portions being very soft. It was composed of connective 
tissue, mucous tissue, fat, sarcomatous tissue, and irregular tubules 
lined with small, polygonal, epithelial cells. Some of the tubules were 
distended with masses of hyalin matter. The whole structure re- 
sembled that of the tumors so often found in the parotid region — 
tumors which can be called " adenoid myxo-sarcomata." 

Carcinomata may originate at any part of the wall of the 
pharynx and oesophagus. They are composed of flat epithelial cells 
closely packed together in masses in the usual way. In the ceso- 



THE ALIMENTARY CANAL. 545 

phagus the new growth begins in the deeper layers of the mucous 
membrane, and grows so as to encircle the tube for a length of one 
or more inches. The tumor remains as a flat infiltration, or it ulcer- 
ates, or it projects inward in large, fungous masses. The growth 
may extend up and down the oesophagus, and even involve the 
pharynx or stomach. 

The ulcerative process may extend outward so as to produce perfo- 
ration into the air passages, the lungs, pleurae, pericardium, and large 
blood vessels. 

The new growth may extend outward and infiltrate the surround- 






'-c/. 



Fig. 268.— Diffuse Sarcoma ok the Pharynx, X 850 and reduced. 

ing soft parts, so that the oesophagus is surrounded by large, solid, 
cancerous masses. Metastatic tumors are also sometimes formed. 

Sarcoma. — I have seen one case in which there was a diffuse growth 
involving both the tonsils, the posterior and lateral walls of the 
pharynx, the base of the tongue, and the epiglottis. The new growth 
replaced the mucous membrane, infiltrated the soft parts for a short 
distance, and projected inward in polypoid masses. It was composed 
of small, polygonal, nucleated cells contained in a very delicate 
nucleated stroma 1 (Fig. 268). 

1 For literature of malignant disease of the tonsils, consult Newman, American 
Journal of the Medical Sciences, May, 1892. Housell, Beitr. zur klin. Chirurgie, 
Bd. xiv. 

44 



546 THE ALIMENTARY CANAL. 

THE STOMACH. 
MALFORMATIONS. 

Malformations of the stomach are not common. The organ may 
be entirely wanting in acephalous foetuses. It may be of various de- 
grees of smallness, sometimes no larger than the duodenum. It may 
be divided into two halves by a deep constriction in the middle. The 
pyloric orifice may be stenosed or entirely closed. The stomach may 
be outside of the abdominal cavity from a hernial protrusion through 
the diaphragm or at some point in the abdominal wall. It is found 
on the right side, instead of the left, when the other viscera are 
transposed, and the position of the cardiac and pyloric orifices is 
correspondingly inverted. 

POST-MORTEM CHANGES. 

In 'adults the stomach after death is of a grayish or pinkish color, 
sometimes mottled with red ecchymoses. The mucous membrane is 
soft and the epithelium easily brushed off. At the fundus the food is 
usually found collected, and here the mucous membrane is the softest. 
It is very common to find the epithelium removed from the entire 
fundus of the stomach, so that all that portion of its wall is grayer 
and thinner, there being a sharp dividing line between the two por- 
tions. Sometimes this post-mortem softening process goes on to de- 
stroy all the coats of the stomach, and even the adjoining portion of 
the diaphragm. In this way the contents of the stomach may be 
emptied into the pleural cavity by a large, ragged opening in the 
stomach and diaphragm. When the softening affects all the coats of 
the stomach the softened portion is not sharply limited. The entire 
thickness of the affected portion of the wall is converted into a gray 
or yellow semi-transparent jelly, or into a blackish, broken-down pulp. 

This softening is most frequent in children, but also occurs in 
adults, usually in connection with severe and exhausting diseases. 

INJURIES. 

Perforating wounds of the stomach usually give rise to a fatal 
peritonitis. It is possible, however, for the wound to heal, or a gas- 
tric fistula may be formed. 

Rupture of the stomach may be produced by severe blows or falls. 

HEMORRHAGE. 

Small extravasations of blood in the wall of the stomach are fre- 
quently found in persons who have died from one of the infectious 
diseases. 



THE ALIMENTARY CANAL. 047 

Haemorrhage into the cavity of the stomach may be produced in 
a variety of ways. 

In ulcers of the stomach there may be bleeding from the small 
vessels of the ulcer or from the perforation of a larger artery. 

In cancer of the stomach there may be bleeding from the tumor. 

Some cases of chronic gastritis are characterized by general bleed- 
ing from the mucous membranes of the stomach. 

Cirrhosis of „ the liver is not infrequently attended with large 
haemorrhages from the mucous membrane of the stomach. 

Small aneurisms of the arteries in the wall of the stomach may 
rupture internally. 

In yellow fever and some of the other infectious diseases there is 
hsemorrhage into the cavity of the stomach. 

Patients may vomit b'j.ood during life, and after death no lesion to 
account for the bleeding be found. 

INFLAMMATION. 

Acute Catarrhal Gastritis, as we see it after death, is usually 
due to the ingestion of irritating substances, or forms part of the 
lesions of cholera morbus. If we can judge from clinical symptoms, 
it occurs during life as a temporary condition from a variety of causes. 

After death the mucous membrane is found congested and swollen, 
or the congestion may have disappeared. The mucous membrane is 
coated with an increased amount of mucus, especially at the pyloric 
end of the stomach. Sometimes there are a number of minute white 
dots in the substance of the mucous membrane. 

The structural changes in the mucous membrane consist simply 
in a swelling of the cells of the gastric tubules, a slight infiltration 
of the stroma with pus cells, and a swelling of the patches of lym- 
phatic cells. The little white dots, when they are present, are com- 
posed of small foci of pus between the gastric tubules, with degene- 
ration and destruction of some of the tubules. 

Chronic Catarrhal Gastritis is a very common disease. There 
is, however, no very close relation between the severity of the symp- 
toms during life and the extent of the lesions found after death. 

In some cases chronic alcoholism, or the abuse of drugs, or the 
mode of life of the patient seems to be the cause of the lesion. 
Chronic phthisis, chronic B right's disease, cirrhosis of the liver, and 
fatty liver are often accompanied by chronic gastritis. Organic dis- 
ease of the heart, or pressure on the ascending vena cava, produces a 
form of chronic gastritis characterized by intense general congestion. 

After death the stomach is found either empty or still containing 
food. It is of normal size, or dilated, or small, sometimes hardly 
larger than the duodenum. Its inner surface is coated with a thick 



548 



THE ALIMENTARY CANAL. 



layer of tenacious mucus, most abundant at its pyloric end. The 
mucous membrane is congested, or white, or slate-colored, or mottled 
with small white spots. It is of normal thickness, or thinned, or 
thickened, or there are little polypoid projections from its surface, or 
there is cystic dilatation of the gastric tubules (Fig. 269). The con- 
nective tissue and muscular coats remain unchanged, or they are 




Fig. 269.— Chronic Gastritis. 
Showing changes in the glandular coat. A small cyst formed by dilatation of a tubule. 



thinned and relaxed, or they are hypertrophied. The hypertrophy 
may be diffuse, or it is confined to the pyloric end of the stomach 
and may then produce stenosis of the pylorus. 

The minute lesions consist principally in changes in the mucous 
membrane. The cells of the gastric tubules are swollen, degenerated, i 
and broken down. The tubules are atrophied and deformed, or di- 
lated into cysts. The patches of lymphatic tissue about the blind 



THE ALIMENTARY CANAL. 549 

ends of the tubules are increased in size. The connective tissue be- 
tween the tubules is infiltrated with cells and increased in quantity. 

Croupous Gastritis is of rare occurrence. It is found in chil- 
dren with croupous inflammation of the pharynx and oesophagus, 
and is then usually in small patches. In adults it is almost always 
secondary to typhus, pyaemia, puerperal fever, cholera, dysentery, the 
exanthemata, and irritating poisons. The false membrane is in 
small patches, or may line a large part of the stomach. The disease 
is usually not diagnosticated during life, the symptoms of the pri- 
mary disease diverting attention from the gastritis. 

I (Delafield) have seen one case of idiopathic croupous gastritis in 
an adult. A man, forty-six years old, was in good health until eight 
days before his death. At that time he caught cold, had pains over 
his bowels, tenderness over the liver, constipation, cough with mu- 
cous expectoration, temperature 102^°, pulse 120. On the day of his 
death, the eighth day of the disease, the temperature was 100°, pulse 
112, tongue dry, abdomen tympanitic and tender, and he died in a 
prolonged attack of syncope. At the autopsy all the viscera were ex- 
amined. Excepting evidences of bronchitis in the lungs, there were 
no lesions save in the stomach. About two-thirds of the internal 
surface of the stomach, including the lesser curvature and anterior 
and posterior walls, appeared to be covered with a thick false mem- 
brane, which did not quite reach to the cardiac or pyloric orifices. 
Minute examination showed that there was a layer of exudation on 
the internal surface of the mucous membrane. This exudation con- 
sisted of fibrillated fibrin and lymphoid cells dipping into the mouths 
of the follicles. Beneath, the exudation the mucous membrane was 
thickened and altered. A large number of lymphoid cells separated 
the follicles, and even replaced them entirely. The submucous layer 
was very much thickened by the presence of lymphoid cells, fibril- 
lated fibrin, and fibrous tissue. The muscular coat was separated 
into layers by groups of lymphoid cells. 

Wilks and Moxon mention a similar case in a man with chronic 
Bright's disease, and a case of both croupous gastritis and colitis 
with abscess of liver. 

Suppurative or Phlegmonous Gastritis. — A formation of cir- 
cumscribed collections of pus may occur in the connective-tissue coat 
of the stomach, as it does in other parts of the body, in puerperal 
fever and the infectious diseases. 

Idiopathic suppurative gastritis is a disease of rare occurrence. 
Leube * has collected thirty- one cases, of which twenty-six were 
males and five females. In some of the cases the inflammation was 

1 Leube, "Ziemssen's Cyclopaedia, " vii., p. 157. 



550 THE ALIMENTARY CANAL. 

ascribed to the excessive use of alcohol, in others to a wound in the 
region of the stomach, in others to some error in diet. 

Fagge 1 describes a case in a male of fifty-one years of age, with- 
out discoverable cause. 

Silcock 2 describes a case in which the gastritis followed the ope- 
ration of gastrostomy. 

I have seen one case occurring in an adult male, without any 
known cause. 

The suppurative inflammation seems to begin in the connective- 
tissue coat of the stomach. From thence it may extend to the glan- 
dular coat and produce perforations, or outward to the muscular and 
peritoneal coats. In some cases there is added a local or general 
peritonitis. 

The inflammation may involve one or more circumscribed areas 
and so produce abscesses, or it may be a diffuse process involving 
the whole extent of the wall of the stomach. 

Toxic Gastritis. — The mineral acids, the caustic alkalies, arse- 
nic, corrosive sublimate, and the metallic salts, phosphorus, camphor, 
and all other irritating materials, cause different lesions of the 
stomach, according to their quantity, their strength, and the length 
of time that has elapsed before death. 

In large quantities they destroy and convert into a soft, blackened 
mass both the mucous membrane and the other coats, so that perfo- 
ration may take place. In smaller quantities they produce black or 
white sloughs of the mucous membrane, surrounded by a zone of in- 
tense congestion. If death does not soon ensue the ulcerative and 
cicatricial processes which follow such sloughs may contract and 
deform the stomach in various ways. 

If the poisons are of less strength they produce a diffused con- 
gestion of the mucous membrane, with catarrhal or croupous exuda- 
tion on its surface and serous infiltration of the submucous coat (see 
chapter on Poisons). 



ULCERS OF THE STOMACH. 

The Chronic Perforating Ulcer. — This form of ulcer is often 
seen ; according to Brinton, in five per cent of persons dying from 
all causes. It occurs in females nearly twice as frequently as in 
males. As regards the age, Brinton concludes that the liability of an 
individual to become the subject of gastric ulcer gradually rises, 

1 Trans. Lond. Path. Soc, 1875, p. 81. 

2 Ibid., 1883, p. 90. 



THE ALIMENTARY CAXAL. 



551 



from what is nearly a zero at the age of ten, to a high rate, which it 
maintains through the period of middle life ; at the end of which 
period it again ascends, to reach its maximum at the extreme age of 
ninety. Lebert gives one hundred and ninety-eight cases in which 
the ulcers were found at the autopsy, as follows : 



15 to 20 years 
20 to 30 years 
30 to 40 years 
40 to 50 years 



NUMBER OF CASES. 



20 

48 
28 
43 



1 50 to 60 years 
60 to 70 years. 
70 to 80 years. 



NUMBER OP CASES. 



2\) 

19 

5 



Hauser 1 gives thirty autopsies from Erlangen of ulcers which 
were still open, as follows : 



20 to 30 years 
30 to 40 years 
40 to 50 years 



NUMBER OP CASES. 



50 to 60 years 
60 to 70 years 
70 to 80 years 



NUMBER OP CASES. 



Moore 2 gives the f ollowing table of the fatal cases of ulcer of the 
stomach occurring at St. Bartholomew's Hospital from 1867 to 1879 : 



SEX. 


AGE. 


POSITION. 


CAUSE OP DEATH. 


M. 
M. 
M. 


36 

19 
47 
47 
41 
52 
46 
47 
57 
19 
40 
46 


Near pylorus 

Greater curve near pylorus. . . 
Near pylorus 


Perforation. 

Haemorrhage. 

Exhaustion. 


M. 
M. 
M. 


Pylorus 

it 


Phthisis. 
Exhaustion. 


M. 
F. 
M. 
M. 
M. 


Lesser curve near pylorus 

Cardiac end 

Near pylorus 


Perforation. 

Sinus in liver to lung. 

Haemorrhage. 

Perforation. 

(C 


F. 


Posterior wall. 


(( 



Goodhardt 3 describes an ulcer of the stomach, which proved fatal, 
from haemorrhage in an infant at birth. 

The situation of these ulcers, according to Brinton, is as follows : 
In 43 per cent, the posterior surface ; in 27, the lesser curvature ; in 
16, the pyloric extremity ; in 6, both the anterior and posterior sur- 
faces ; in 5, the anterior surface only ; in 2, the greater curvature ; 
in 2, the cardiac pouch. Thus about 86 ulcers in every 100 occupy 
the posterior surface, the lesser curvature, and the pyloric sac. 

The analysis of 793 hospital cases by Welch shows that the ulcers 



1 "Das chron.'Magengesch., " 1883. 

Ibid. 



2 Trans. Lond. Path. Soc, 1880, p. 110. 
1881, p. 79. 



552 THE ALIMENTARY CANAL. 

were on the lesser curvature in 288, in the posterior wall in 235, at 
the pylorus in 95, on the anterior wall in 00, at the cardia in 50, at 
the fundus in 29, on greater curvature in 27. 

As regards the number of ulcers, two or more are present in about 
twenty- one per cent ; there may be two, three, four, or even five 
ulcers. In cases of multiple ulcers the ulcers are often developed 
successively. 

In size the ulcers vary from one-quarter of an inch to five or six 
inches. 

They are usually of circular shape, sometimes oval ; sometimes 
two or more are fused together. 

The perforation is largest in the mucous membrane. It may re- 
main confined to this, or extend outward and involve the connective 
tissue, muscular and peritoneal coats, its diameter becoming smaller 
as it advances. The ulcer looks like a clean hole punched out of the 
wall of the stomach. Its floor shows no active inflammatory changes. 
Its edges may be in the same condition, or they may be thickened by 
the growth of connective tissue and cells. The rest of the mucous 
membrane of the stomach is apt to be in a condition of chronic ca- 
tarrhal inflammation. 

The ulcer may perforate directly through the wall of the stomach, 
and the contents of the latter are discharged into the peritoneal cav- 
ity ; or adhesions are formed between the wall of the stomach and 
the neighboring viscera, so that the bottom of the ulcer is closed ; or 
if the liver, the intestines, or the abdominal wall become adherent, 
they may be invaded by the ulcerative process, and cavities or fistu- 
lse are formed communicating with the stomach ; or, if the adhe- 
sions are incomplete, a local peritonitis and collections of pus may be 
developed. 

During the progress of the ulcer there may be repeated small 
haemorrhages from the erosion of small blood vessels, or large haem- 
orrhages from the erosion of large arteries. 

In many cases these ulcers cicatrize, and such a cicatrization may 
produce various deformities of the stomach. 

It is very difficult to understand how these ulcers are produced. 
It seems probable that the nutrition of a circumscribed part of the 
wall of the stomach is interfered with, and that this portion is then 
destroyed by the action of the gastric juice, But we are still igno- 
rant of the way in which the obliteration of the arteries is effected. 
It has, indeed, been demonstrated in animals that an artificial em- 
bolism of the branches of the gastric arteries will produce ulcers of 
the stomach ; and in the human stomach we occasionally meet with 
cases of embolism of the branches of the gastric artery and ulcers. 
But the clinical history of most cases of ulcer of the stomach will 



THE ALIMENTARY CANAL. 



553 



not correspond with such a method of causation. A chronic oblite- 
rating endarteritis would seem to be a more probable cause. 

Hemorrhagic Erosions occur as rounded spots or narrow 
streaks, formed by a loss of substance of the mucous membrane. 
The mucous membrane at these points is congested, soft, and cov- 
ered by small blood clots. The destruction of the mucous mem- 
brane is usually superficial, but may involve its entire thickness. 
The number of these erosions may be so great that the entire inter- 
nal surface of the stomach is studded with them. They give rise to 
repeated haemorrhages, and are accompanied by catarrhal inflamma- 
tion of the rest of the mucous membrane. 

They occur at all periods of life, even in infants. Their usual 
seat is the pyloric portion of the stomach. 




Fig. 270.— Superficial Necrosis op the Mucous Membrane op the Stomach— Child. 

They may be idiopathic. Usually, however, they occur in con- 
nection with some serious general disease. 

Follicular Ulcers somewhat resembling the ulcers of the small 
intestine are occasionally met with. They are produced by changes 
in the aggregations of lymphatic tissue which are situated about the 
blind ends of the gastric tubules. 

I have seen in the stomach of a child numerous small ulcers 
formed by a superficial necrosis of the glandular coat. There were 
similar ulcers in the colon. There was no clinical history (Fig. 270). 



DILATATION. 

Very considerable degrees of dilatation of the stomach are found 
at autopsies, without stenosis of the pylorus or any other mechanical 
cause to account for them. It is usually difficult to determine how 
long these dilatations have existed and how much effect they have 
in causing death. ISTine such cases are recorded by Goodhardt. 1 

Acute Dilatation of the stomach, with vomiting of very large 

1 Trans. Lond. Path. Soc, 1883, p. 88. 



554: 



THE ALIMENTARY CANAL. 



quantities of thin fluid, has been observed in a few cases. 1 It is a 
very curious condition, the dilatation of the stomach being developed 
suddenly and without discoverable cause. 

Of the mechanical causes which produce dilatation of the stomach, 
a stenosis of the pylorus is the most common. Such a stenosis may 
be effected by a tumor, by chronic inflammation and thickening, and 
by the cicatrization of ulcers. Less frequently obstructions of the 
small and large intestines act in the same way. 

Some forms of chronic gastritis are attended with dilatation of 
the stomach without stenosis. 




Fig. 271.— Fibroma in the Wall of the Stomach op a Child, 
There were several of these small tumors in the wall of the stomach. 



In rare cases circumscribed, sacculated dilatations are produced 
by the presence of foreign bodies — portion of wood, metal, etc. 



TUMORS. 

Papilloma. — It has already been mentioned that in some cases 
of chronic gastritis there are small, polypoid hypertrophies of the 
mucous membrane. Besides these we find polypoid tumors which 
may reach a considerable size. They are composed of a connective- 
tissue stroma arranged so as to form tufts covered with cylindrical 
epithelium. In some cases there are also tubules lined with cylin- 
drical epithelium, so that the tumor has partly the structure of an 
adenoma. Fibromata of small size are sometimes found in the con- 



Ibid., vol. iv. and vol. xxxiv., p. 82. Hughes Bennett, "Practice of "Medicine. " 
Guy's Hospital Reports, vol. xviii. , p. 1. Andral, Clinique Medicale. 



THE ALIMENTARY CANAL. 000 

nective-tissue coat. Lipomata are formed in the submucous con- 
nective tissue in the shape of rounded or polypoid tumors. They 
usually project inward, but sometimes outward beneath the perito- 
neum. They may also appear in the form of numerous yellow nod- 
ules beneath the mucous membrane. 

Myomata occur in the form of rounded tumors which originate 
in the muscular coat, but may gradually separate themselves from it 
and project inward or outward. The submucous myomata are at 
first small tumors lying loosely attached in the submucous tissue. 
As they grow larger they push the mucous membrane inward and 
take the shape of polypoid tumors. Lymphomata in the wall of the 
stomach are seen in some cases of leukaemia. 

Sarcomata are said to occur in the wall of the stomach in rare in- 
stances. It must be admitted that in some of the tumors of the wall 
of the stomach, which are ordinarily called cancerous, the structure 
is not well defined, and it is possible that some of them are sarco- 
mata. 

A myo-sarcoma growing outward from the greater curvature of 
the stomach is described by Brodowski. 1 The tumor weighed twelve 
pounds. It was composed largely of smooth muscle cells. There 
was a secondary tumor in the liver. 

Adenoma. — It has been already mentioned that in some of the 
papillary tumors of the mucous membrane there is a considerable 
growth of tubules lined with cylindrical epithelium. 

Besides these we find in the submucous coat circumscribed tumors 
composed of tubules like those of the gastric mucous membrane. 

Small tumors resembling the pancreas have also been seen in the 
submucous and subserous coats. 

Carcinoma of the stomach is almost always primary. But very 
few secondary cases have been recorded. 2 

Primary carcinoma of the stomach is of the colloid variety, or 
common cancer, or cancer with cylindrical epithelial cells, or it is pig- 
mented. 

Colloid cancer is composed of a connective-tissue stroma, arranged 
so as to form cavities of different sizes, which contain colloid matter 
and polygonal cells. It infiltrates first the submucous connective 
tissue and then extends inward and outward. In this way there is 
formed a diffuse thickening of the pyloric end of the stomach rather 
than a circumscribed tumor. Sometimes the whole of the wall of the 
stomach is changed in this way. Secondary tumors are usually situat- 
ed in the peritoneum. 

1 Virch. Arch., Bd. lxvii., p. 227. 

2 Ibid., Bd. xxxviii. and lxxxvi., p. 159. Trans. Path. Soc, London, 1876, p. 264. 



556 THE ALIMENTARY CANAL. 

Carcinoma with cylindrical epithelial cells. These tumors are 
formed of a connective-tissue stroma, which may contain numerous 
round cells, and of tubules lined with cylindrical epithelium like that 
of the mucous membrane of the stomach. In these tumors the new 
growth seems to begin in the gastric tubules. As the arrangement 
of the tubules is more or less regular, these tumors may be called 
adenomata or carcinomata (see Fig. 147). 

Common cancer is formed of a connective-tissue stroma enclosing 
rounded and tubular spaces filled with small, polygonal, nucleated 
cells. In some cases this structure is well marked. In others the 
stroma is abundant and filled with round cells, the spaces are very 
small, and the epithelial cells few ; it may then be difficult to distin- 
guish between inflammatory thickening, sarcoma, and carcinoma. 

Both these forms of carcinoma, common cancer and cancer with 
cylindrical cells, run the same course as regards their gross appear- 
ance, their situation, and their development of metastatic tumors. 

About sixty per cent of these tumors are situated at the pyloric 
end of the stomach, on the lesser curvature or on the posterior wall. 
The cardiac end of the stomach, the greater curvature, or nearly the 
entire wall of the stomach may also be the seats of the new growth, 
but not as frequently. 

The new growth usually follows one or other of three types. 

1. There is a circumscribed, flat tumor formed in th3 deeper 
layers of the mucous membrane and pushing this membrane inward. 
After a time the mucous membrane over the centre of the tumor 
dies, the destructive process involves the tumor also, and so an ulcer 
with thickened edges is formed. In some cases the new growth ex- 
tends laterally and outward, while the central destruction still con- 
tinues ; then the ulcers reach a large size, their walls and floor are 
thick, and peritoneal adhesions are formed over them. In other cases 
the ulcer perforates completely through the wall of the stomach, un- 
less the opening is closed by adhesions to the neighboring viscera. 

2. Large rounded tumors are formed, often several inches in dia- 
meter, which project into the cavity of the stomach. 

3. There is a diffuse, flat infiltration of the deep layers of the mu- 
cous coat, of the connective-tissue coat, and sometimes of the muscu- 
lar coat, which does not ulcerate and hardly forms a tumor. This 
infiltration may be confined to the pyloric end of the stomach, or 
may involve nearly the whole of its wall. 

There is in most of the cases a good deal of chronic catarrhal in- 
flammation of the mucous membrane. 

If the pylorus is obstructed the stomach is often dilated. . 

The new growth may extend from the stomach to the oesophagus, 
but it very seldom involves the duodenum. 



THE ALIMENTARY CANAL. 557 

Metastatic tumors are very common. The liver, the lymphatic 
glands, and the peritoneum are the parts most frequently affected, 
but such metastases have been seen in nearly every part of the body. 

DEGENERATIONS. 

Calcification of the mucous membrane of the stomach some- 
times occurs as a metastatic process in connection with extensive 
diseases of the bones. 

Waxy Degeneration sometimes involves the blood vessels of the 
mucous membrane. 

FOREIGN BODIES. 

Among the various foreign bodies which by accident or design 
may be present in the stomach may be mentioned hairs, thread, 
string, etc., which having been swallowed from time to time, usually 
by hysterical women. These may be closely packed together into 
a large mass nearly filling the cavity of the stomach, to which in 
shape it may correspond. Such a specimen of gastric hair ball, men- 
tioned by Osier, is in the museum of McGill University, and another, 
reported by Findler, is in the museum of the J College of Physicians 
and Surgeons, New York. 

THE INTESTINES. 

MALFORMATIONS. 

Diverticula of the intestines occur in several different ways : 

1. The abdominal walls are cleft asunder at the navel. The ileum 
opens through this cleft by a narrow aperture in its wall. The lower 
portions of the ileum and the colon are small or entirely closed. 

2. There is an opening in the abdominal wall as before, but there 
is not a direct opening into the ileum. There is a long diverticulum 
of the ileum, with an open end projecting into the opening in the ab- 
dominal wall. 

3. The abdominal wall is closed. There is a diverticulum of the 
ileum, connected with the navel by a solid cord. 

4. There is an unattached diverticulum of the intestine. This is 
much the most common form. The diverticula occur only in the 
lower part of the ileum. They usually spring from the convex sur- 
face of the intestine, more rarely from its attached border. In the 
latter case they are joined to the mesentery by a fold of peritoneum. 
The diverticulum forms a pouch, one to six inches long, of about the 
same diameter as the intestine, smallest at its free extremity. 

Such diverticula do not interfere with the functions of the intes- 
tines. They sometimes form part of a hernia. Sometimes the remains 



558 THE ALIMENTARY CANAL. 

of these intestinal diverticula — called Meckel's diverticula — form soft, 
projecting tumors at the umbilicus in children. Microscopical exam- 
ination of such tumors often shows the structure of the intestinal 
mucosa and muscularis. If they remain attached by a fibrous cord 
to the navel, this cord may be the cause of incarceration of a portion 
of the intestines. 1 

Cloacae consist in the union of the rectum, bladder, and organs of 
generation in a common outlet. 

1. Simple Cloacce are : (a) Complete, and consist in the common 
opening of the urethra or ureters, the vagina, and the rectum into 
the closed bladder, or into a sinus opening outward which represents 
either the vagina or the rectum, (b) Incomplete. The rectum opens 
into the vagina, the bladder, or the urethra, while the lower part of 
the rectum is closed or absent. 

2. Cloacce combined with Cleft Bladder, — (a) The simple cleav- 
age of the intestines is combined with cleft bladder. The anterior 
abdominal wall from the umbilicus to the symphysis, the symphysis, 
and the anterior wall of the bladder are absent ; the gap is filled with 
a membrane which represents the posterior wall of the bladder. On 
to this membrane open the ileum, ureters, and vagina, (b) The intes- 
tine is perfectly formed, but the rectum opens into a common sinus 
with the ureters and vagina ; or the ureters open into the cleft blad- 
der, and the rectum and external genitals are united ; or the ureters 
open into the rectum, and the latter terminates normally. 

3. Cloacce combined with Abdominal Hernia. — There is a her- 
nial sac containing all the abdominal viscera. At the lower end of 
the sac is an opening leading into a sinus in which open the lower 
end of the ileum, the bladder or urethra, and the ureters. The rec- 
tum is absent. 

Atresia Ani consists in a deficient development of the colon or 
rectum. The entire colon may be absent ; the rectum may be absent, 
or represented by a solid cord ; or the upper or lower part of the 
colon may be absent, or separated by a solid cord. 

More rarely blind terminations of the small intestines are found, 
and sometimes a narrowing so complete as to close the canal. 

The intestines are also found abnormally shortened in various de- 
grees. A colon of unusually large size has been described as of 
occasional occurrence.' 2 

INCARCERATION. 

1. The most common form is that in which a portion of intestine 
is strangulated by a fibrous band. Such fibrous bands are produced 

1 For false intestinal diverticula, see p. 577. 

* Formad, University Medical Magazine, June, 1892. 



THE ALIMENTARY CANAL. 559 

by peritonitis or the remains of foetal growth. They pass from the 
intestines to the abdominal wall, or from one part of the intestines to 
another. The intestine becomes in some way caught under one of 
these bands and is compressed by it. The stricture thus produced 
may cause a gradual accumulation of fseces in the intestine above it, 
and may last for a long time before death ensues. In other cases the 
stricture interferes at once with the circulation of the blood ; the in- 
testine is intensely congested, becomes gangrenous, and death takes 
place with the symptoms of general peritonitis. 

2. A portion of intestine becomes caught in some abnormal open- 
ing in the mesentery or omentum, or in the foramen of Winslow, or 
between the two layers of the mesentery. We have seen a case in 
which twelve feet of intestine had passed through a small opening in 
the mesentery. 

3. A coil of intestine makes half a turn at its base, so that the 
two sides of the loops cross at its base. In this way the lumen of 
the intestine is completely closed and the vessels are compressed, so 
that congestion, peritonitis, and gangrene result. This form of in- 
carceration is most frequent in the ascending colon. In the small 
intestine it only occurs when the gut is fixed by old adhesions. 

4. A portion of the intestine, with its mesentery, makes one. or 
more complete turns on itself, closing the canal and compressing the 
vessels. 

5. A portion of the intestine makes a half or entire turn about its 
longer axis. This is very rare, and only occurs in the colon. 

6. The mesentery of a part of the intestine is long and loose, in 
consequence of a dragging down of the intestine by a hernia or by 
habitual constipation. The portion of intestine thus permitted to 
hang down is habitually filled with fseces, and by its pressure on 
some other part of the intestine produces an incomplete stricture. 

INTUSSUSCEPTION. 

This change of position consists in the invagination of one por- 
tion of intestine in another portion. Usually this takes place in the 
direction of the peristaltic movements, from above downward ; more 
rarely in the opposite direction. 

The parts are found in the following condition : There are three 
portions of intestine, one within the other. The inner portion is 
continuous with the intestines above the intussusception ; its peritoneal 
coat faces outward. The outer portion is continuous with the intes- 
tine below ; its peritoneal coat also faces outward. The inner portion 
is turned inside out, its mucous membrane is in contact with the 
mucous membrane of the outer portion. In rare cases the intus- 
susception is complicated by the invagination of a second portion of 



560 THE ALIMENTARY CANAL. 

intestine in the inner tube, and even by a third intussusception into 
the second one. These changes occur both in the large and small 
intestine ; most frequently the lower part of the ileum is invagi- 
nated in the colon. The invaginated portion may be from a few 
inches to several feet in length. The lesion is most frequently found 
in early childhood. 

The intussusception, by the dragging and folding of the mesen- 
tery which it produces, causes an intense congestion of the parts, and 
even large haemorrhages between the coats of the intestine. The 
congestion may induce fatal peritonitis, or gangrene of the intestine, 
or chronic inflammation and adhesions, and the patient lives for a 
considerable time with symptoms of stricture. In other cases the 
invaginated portion of intestine sloughs, the outer and inner portions 
become adherent, and the patient recovers, with or without some de- 
gree of stricture. 

Besides this grave form of intussusception we often find, es- 
pecially in children, one or more small invaginations not attended 
with congestion or inflammation. These are formed during the death 
agony or immediately after death. 

TRANSPOSITION. 

The position of the intestines may be the opposite to that which 
is usually found. The transposition may affect all the abdominal 
viscera, or only a single viscus is transposed. 

WOUNDS — RUPTURES. 

Penetrating wounds of the intestine usually prove rapidly fatal, 
either from shock or from peritonitis. Sometimes, however, the 
wound becomes closed by the formation of adhesions with the 
neighboring parts. Sometimes the wound in the intestines becomes 
adherent at the position of the wound in the abdominal wall, and an 
intestinal fistula is formed. 

Rupture of the small intestine is not infrequently produced by se- 
vere blows on the anterior abdominal wall. It is noticeable that such 
blows may not produce any marks or ecchymoses of the skin. Such 
ruptures usually prove fatal very soon, but sometimes the patient 
lives several days and the edges of the rupture undergo inflamma- 
tory changes. 

Strictures of the intestine are sometimes followed by rupture of 
the dilated intestine at some point above the stricture. 



THE ALIMENTARY CANAL. 561 

THE SMALL INTESTINE. 
INFLAMMATION. 

Acute Catarrhal Inflammation of the greater part of the small 
intestine is developed as part of the lesion of cholera morbus, and 
after the ingestion of irritant poisons. 

Acute inflammation of the duodenum accompanies gastritis, and 
occurs as an idiopathic condition. 

Acute inflammation of the ileum occurs as an idiopathic condi- 
tion, and accompanies inflammation of the colon and of the solitary 
and agminated lymph nodules. 

In many of these cases we infer the existence of the inflamma- 
tion from the clinical symptoms. 

After death the most marked lesions are the increased produc- 
tion of mucus and the congestion. In very severe cases the inflam- 
mation may extend to the peritoneal coat. 

Chronic Catarrhal Inflammation of the small intestine accom- 
panies heart disease, phthisis, emphysema, cirrhosis of the liver, and 
Bright's disease. The intestine is coated with an increased amount 
of mucus ; it is often congested ; there may be a general thickening 
of all its coats. 

Croupous Inflammation is produced by irritant poisons; it is 
associated with croupous colitis, and it occurs as an idiopathic disease. 
The mucous membrane is coated with fibrin, its stroma is infiltrated 
with fibrin and pus, and this infiltration extends to the connective 
tissue, muscular and peritoneal coats. 

Suppurative Inflammation of the submucous connective-tissue 
coat is said to occur in rare cases. It is usually metastatic. It takes 
the form of purulent foci of variable extent, which perforate either 
inward or outward. 

THE SOLITARY AND AGMINATED GLANDS (LVMPH NODULES). 

It is not uncommon to find in healthy adults who have died from 
accidental causes a considerable swelling of the solitary and agmi- 
nated glands (lymph nodules) of the ileum, without any reason 
which we can discover to account for this swelling. 

Extensive burns of the skin may be followed by a very marked 
swelling of the solitary and agminated nodules. 

In persons who have died from the infectious diseases it is not 
uncommon to find these nodules swollen. 

In children, swelling of these nodules, often followed by softening 
and the formation of ulcers, accompanies many of the catarrhal in- 
flammations of the large arid small intestines. 
15 



562 THE ALIMENTARY CANAL. 

In pulmonary phthisis we very frequently find changes in the 
solitary and agminated nodules of the small intestine, less frequently 
in the solitary nodules of the colon. The changes seem to be of the 
same character as those which take place in tubercular inflammation 
of lymphatic nodules in other parts of the body. 

The nodules become swollen, their elements are multiplied, tuber- 
cle granula are formed, the central portions of the nodules become 
cheesy. The cheesy degeneration extends ; it is followed by soften- 
ing and by death of the mucous membrane over the nodules ; the 
softened tissue is discharged into the intestine, and ulcers are formed 
with overhanging edges. After this the ulcer shows no tendency to 
heal, but, on the contrary, becomes larger, usually extending late- 
rally so as sometimes to nearly encircle the gut. After death we 
find, in different patients, these ulcers in all their stages of develop- 
ment. They vary much as to the proportion between the tubercular 
and the ordinary inflammatory changes. In some the tubercle 
granula are numerous, in others they are few or even absent alto- 
gether. The tubercle bacilli are very constantly found in them. 
There is also usually a tubercular inflammation of the peritoneum 
over the ulcers, and sometimes of the lymphatics and nodes of the 
mesentery. Although these ulcers often reach a large size, it is but 
very seldom that they perforate into the peritoneal cavity. 

Ulcers of the Duodenum. — A few cases have been recorded in 
which extensive burns of the skin have been followed within a few 
days by the formation of deep ulcers of the duodenum. It is still 
uncertain how these ulcers are produced. 

Chronic perforating ulcers, resembling the chronic ulcers of the 
stomach, are found in the duodenum. They are associated with 
similar ulcers in the stomach or occur by themselves. 

Some curious ulcers of the upper part of the small intestines are 
described by Israel. 1 There were five ulcers, from two and one-half 
to ten centimetres long, encircling the intestine, with irregular, 
granulating surfaces. 

Syphilitic ulcers produced by changes in the solitary and agmi- 
nated glands of the small intestine are sometimes found in infants. 

EMBOLI. 

Emboli have been found in the superior mesenteric artery in a 
number of cases ; in the inferior mesenteric artery they are less fre- 
quent. They produce an intense venous congestion of the entire 
wall of the intestine, with hemorrhage into its cavity and its wall. 

1 Charite-Annalen, 1384, p. 707. 



THE ALIMENTARY CANAL. 



563 



THE LARGE INTESTINE. 
INFLAMMATION. 



The mucous membrane of the large intestine is very frequently 
the seat of acute and chronic inflammatory processes. The larger 
number of these belong to the condition which is described clinically 
under the name of dysentery. The inflammation affects most fre- 




Fig. 272. — Acute Catarrhal, Colitis. 

With mucus on the surface of the mucous membrane, distending the tubules and filling some of 
the cells (beaker cells). 



quently the rectum, sometimes the entire length of the colon, some- 
times only the upper part of the colon. 

Acute Catarrhal Colitis. — The lower end of the colon is the por- 
tion most frequently involved in this form of inflammation, but it 
may be its upper end or the entire length of the gut. The name ca- 



564 



THE ALIMENTARY CANAL. 



tarrhal colitis is the only term used at the present time to designate 
three morbid conditions of the colon, which differ from each other 
both in their anatomical and clinical features. 

1. The inflammation is of simple exudative type. It is usually 
confined to the lower end of the colon, runs its course within a week, 
and is not fatal. The glandular and connective-tissue coats of the 
colon are swollen and congested, with more or less infiltration with 




Fig. 273.— Suppurative Colitis. 

The inflammation is confined to the connective-tissue coat, causing destruction of large por- 
tions of this coat, thus undermining the glandular coat. The photograph is from a vertical section 
through the whole wall of the colon, and shows a separation of the glandular from the vascular 
coat. 

serum aud pus cells. There is an increased production of mucus 
(Fig. 272) which coats the surface of the colon and comes away 
with the stools in the form of membranes or cord-like shreds. 1 There 
may be bleeding from the surface of the inflamed mucous membrane. 



Numerous observations have been made and a large bibliography has been 
gathered on what is called membranous enteritis or colitis, for which the reader may 
consult Butler, New York Medical Journal, December 28th, 1895, or ' Akerlund > 
Arch. f. Verdauungs Krankheiten, Bd. i., p. 396, 1896. 



THE ALIMENTARY CANAL. 



565 



2. The inflammation is of exudative type, but with an excessive 
production of pus cells. It may involve any part of, or the entire 




Fig. 274,— Catarrhal Colitis. 
Showing swollen lymph nodule. 








Fig. 275.— Catarrhal Colitis, productive and necrotic. 

length of, the colon. It may cause death within a few days or con- 
tinue for several weeks. The wall of the colon is swollen and con- 



566 



THE ALIMENTARY CANAL. 



gested. The stroma between the tubules, the connective-tissue coat r 
and sometimes the muscular and peritoneal coat are infiltrated with 
large numbers of pus cells (Fig. 273). The solitary nodules may be 
swollen (Fig. 274). There is an increased production of mucus. 

3. The inflammation is of the productive type with exudation. It 
may involve any part, or the entire length, of the colon. It may 
cause death within a few days, or continue for several weeks, or be 



\ 



/ 








-«-*' 



Fig. 276.— Croupous Colitis. False membrane in patches. 

followed by chronic colitis. The wall of the colon is swollen and 
congested. There is an increased production of mucus. There is 
a growth of new connective tissue with an excess of cells, confined to 
the stroma between the tubules or also involving the connective- 
tissue coat. 

4. There may be also a considerable production of pus cells, which 
are found adherent to the surface of the mucous membrane and infil- 
trating the glandular and connective-tissue coats. In addition we 



THE ALIMENTARY CANAL. 



567 



find numerous small ulcers in the glandular coat. The ulcers are 
often so small that they cannot be seen with the naked eye. They 
seem to be formed by necrosis of small areas of the glandular coat 
(Fig. 275). 

Croupous Colitis. — This form of inflammation may involve the 
rectum alone, or the entire length of the colon, or only its upper por- 
tion. The mucous membrane is congested and swollen, and coated 




Fig. 277.— Follicular (Nodular) Colitis. 

with a layer of false membrane ; the connective tissue between and 
beneath the glandular tubules is infiltrated with fibrin and pus, and 
in severe cases the inflammation involves the muscular and peri- 
toneal coats also. The inflammation is usually more intense at some 
places than at others, so that the surface of the mucous membrane 
shows the false membrane in isolated patches (Fig. 276). Less fre- 
quently there is a uniform coating with the false membrane. In mild 
cases, as the inflammation subsides, the products of inflammation are 



THE ALIMENTARY CANAL. 



absorbed and the wall of the intestine returns to its normal condition 
In more severe cases the quantity of the inflammatory products is so 
great that portions of the wall of the intestine become necrotic. This 
necrosis may involve only the glandular coat, or it may extend deeper 
into the wall of the intestine. The necrosed tissue after a time sloughs 
away, leaving behind ulcers of different sizes and depths. After this 
the ulcers may cicatrize, or their floors and walls may remain in the 
condition of granulation tissue for an indefinite length of time. When 




Fig. 278. — Amcebic Colitis. 
Connective-tissue coat of the intestine infiltrated with new cells and with amoebae. The larger 
spherical structures in the section are sections of bloodvessels; the smaller darker nuclei belonging 
to the new -formed tissue cells; the spheroidal nucleated structures of intermediate size are the 
amoebae. 

the latter is the case there is added a chronic inflammation of the 
wall of the intestine between the ulcers, with changes in the mucous 
membrane and thickening of the connective-tissue and muscular 
coats. 

Follicular Colitis (Nodular Colitis) . — In many cases of catarrhal 
and croupous inflammation of the colon the solitary follicles (lymph 



THE ALIMENTARY CANAL. 



569 



nodules) become more or less swollen and necrotic. Besides these 
cases, however, there are others in which the changes in the nodules 
form the principal part of the lesion, while the catarrhal or croupous 
inflammation is but slightly developed. The nodules are first 
swollen, then necrotic, then slough away and leave little circular 
ulcers with overhanging edges (Fig. 277). These ulcers are usually 
numerous and extend over a large part of the colon. The patients 
have diarrhceal rather than dysenteric passages. The ulcers are apt 



,-< 




] » V.t 



/ 



Fig. 279.— Amceeic Colitis. 
Showing amoebae in connective tissue. Magnified 1 ,000 diameters and reduced. 

to show but little disposition to heal, and the acute colitis often be- 
comes chronic. It seems probable that some of the cases which look 
like follicular colitis are really examples of amoebic colitis. 

Amoebic Colitis.— This form of colitis is caused by the presence 
in the wall of the intestine of amoebae. These organisms were first 
recognized by Lambl in 1859. Since then they have been described 
by a number of observers, most fully by Kartulis and by Councilman 
(see page 128). 



570 



THE ALIMENTARY CANAL. 



The amoebae are found in the little, gelatinous masses which are 
found in the stools. They are of rounded shape, and, when alive, 
change their position and shoot out and retract little projections 
(pseudopodia) . Their outer portion is composed, of a pale hyalin or 
homogeneous substance; the inner contains vacuoles and is more 
refractive (see Fig. 30). 

In the colon the amoebae are found in the connective-tissue coat 
and in the floors of the ulcers (Figs. 278 and 279). The principal 




Fig. 280.— Amcebic Colitis — twelve days' duration. 
A deep ulcer with overhanging edges formed by circumscribed necrosis. 

effect of the presence of the amoebae seems to be to cause the death of 
tissue. The addition of inflammatory changes seems to depend upon 
an additional infection with streptococci, or other micro-organisms. 
As an amoebic colitis may last for many months and as the same pa- 
tient may have a number of attacks, by the time of death the changes 
in the colon are very considerable. The cases which have come 
under our observation have followed one of these anatomical types. 
(a) There is a diffuse inflammation of exudative and productive 



THE ALIMENTARY CANAL. 



571 



type which involves a considerable part of the colon. The cnanges 
are confined to the glandular and connective-tissue coats. In the 
glandular coat there is a growth of new connective tissue and an 
infiltration of pus cells between the tubules. In the connective-tissue 
coat we find new connective-tissue cells, pus cells, and amoebae. The 
ulcers are superficial and involve only the glandular coat. We find 
also in many places portions of the glandular coat which are necrotic, 
but have not sloughed away. 

(b) There are foci of circumscribed exudation and necrosis scat- 




" - \ +■ '■ ' V v* %£ 



._.\, 



- 



__.._,_.._ -3 



Fig. 281.— Amoebic Colitis. 
Showing diffuse necrosis of glandular coat. 



tered through the colon. These foci begin in the connective-tissue 
coat, but may be so large as to involve all the other coats of the colon. 
The exudation forms a sort of nodule which soon becomes necrotic 
and sloughs away, leaving a deep ulcer with overhanging edges (Fig. 
280). The amoebae are found in the walls and floors of the ulcers. 
The glandular coat between the ulcers shows various changes due to 
catarrhal and productive inflammation. 

(c) Considerable areas of the glandular, connective-tissue, and 
muscular coats are necrotic. The dead tissue is found still in place, 
or has sloughed away, leaving very large and deep ulcers (Fig. 281). 



572 



THE ALIMENTARY CANAL. 



In some cases of amoebic colitis necrotic and inflammatory changes 
of the same character are found in the liver and in the right lung. 

Necrotic Colitis. — There is a form of inflammation of the colon 
in which considerable areas of the connective-tissue coat become 
necrotic, leaving the glandular coat undermined and separated from 
the muscular coat. In this way large ulcers with overhanging edges 
are formed. This form of colitis is very fatal. 

There is another very fatal and obscure form of necrotic colitis in 
which the symptoms are rather of septic poisoning than of inflam- 







.■■■'■ 






Mritjiitf'ii 


























'",,, •• '? : 








~; '' «**«*»», 













Fig. 5*82.— Necrotic Colitis. 
Circumscribed congestion and necrosis of the glandular and connective-tissue coats. 



mation of the colon. After death the inner surface of the colon is 
found studded with little blackish swellings. In these swellings the 
blood vessels are gorged with blood. The glandular and connective- 
tissue coats are infiltrated with pus cells and there is a superficial 
necrosis (Fig. 282). 

Various forms of micro-organisms have been found in connection 
with suppurative and necrotic lesions of the colon: Streptococcus 
pyogenes, Staphylococcus pyogenes, Bacillus coli communis, Ba- 
cillus proteus, Bacillus pyogenes, and others. 



THE ALIMENT AEY CANAL. 573 

The exact significance of these germs is yet obscure. 1 

Chronic Colitis. — If a chronic inflammation of the colon has 
continued for any length of time, the wall of the gut is found to be 
very much changed. The glandular coat may be uniformly thick- 
ened, or thrown into the form of polypoid tumors, or atrophied, or 
destroyed by ulcers of various sizes and shapes. The connective- 
tissue and muscular coats may be thickened or thinned. Apparently 
chronic colitis may follow any of the forms of acute colitis. 

The Ccecum. — Catarrhal inflammation of the caecum is not un- 
common. It is usually produced by an habitual accumulation of 
faeces in this part of the intestine. The course of the inflammation 
is chronic, but marked by acute exacerbations. At first the mucous 
membrane undergoes the ordinary changes of chronic catarrhal in- 
flammation; then there is a slow suppurative inflammation which 
extends through the wall of the intestine and produces ulcers and 
perforations. Through these perforations the faeces may pass into 
the peritoneal cavity, or the perforations are partly closed by adhe- 
sions, and abscesses are formed, or sinuses into the surrounding soft 
parts. 

The Rectum. — Besides the inflammatory changes already de- 
scribed as existing in the colon, we sometimes find a suppurative 
inflammation of the connective tissue which surrounds the rectum, 
either associated with lesions of the mucous membrane or occurring 
by itself. 

In adults the lower end of the rectum is the part of the intestine 
which is the most frequent seat of syphilitic ulceration. Most of 
these ulcers seem to be the result of unnatural coitus, or of infection 
from specific sores of the vulva; but some of them seem to be due to 
the softening of gummy tumors. 

The Vermiform Appendix. — The appendix is given off from the 
inner and posterior aspect of the lower end of the caput coli. It is 
from two to six inches in length. It may be turned upward behind 
the caecum, or it may hang downward free in the peritoneal cavity. 
It is composed of peritoneal, muscular, connective-tissue, and glan- 
dular coats. 

1. The mucous membrane may be the seat of acute catarrhal in- 
flammation. This is of mild t}'pe and short duration, with conges- 
tion, swelling, and an increased production of mucus; or it is of 
severer type, of longer duration, and the cavity of the appendix is 
distended by large quantities of mucus and pus. 

2. The entire thickness of the wall of the appendix may be the 
seat of an acute exudative inflammation. The appendix is verj- 

x See Kruse and Pasc/uale, Zeits. f. Hygiene und Infkr., Bd. xvi., p. 1, 1894; 
also Cerenville, Tavel, and others, Ann. Suisses des Sc. 3Ied., ser. ii., p. 531, 1895. 



574 THE ALIMENTARY CANAL. 

much increased in size, sometimes to the size of a man's finger. This 
increase in size is due, not to a dilatation of the cavity of the appen- 
dix, but to a thickening of its walls. The walls are congested, 
swollen, infiltrated with fibrin and pus, the peritoneal coat covered 
with fibrin. There is no necrosis and no perforations. If the appen- 
dix is behind the csecum, or if adhesions are formed early, there is 
only a localized peritonitis. If the appendix projects freely into the 
peritoneal cavity and no adhesions are formed, a general peritonitis 
is soon established. 











mmm$' 



■. - t.r' 

-. : ■■■;■■■■■■■ 

-- ■■■-. wmmM--i k 



2 mBs?- 



Fig. 283.— Acute Suppurative Appendicitis. 
Appendix removed by operation twelve hours after first symptoms. Streptococcus was found 
in the exudate. (Specimen prepared by Dr. Van Gieson.) 1, Mucous membrane of the appendix; 
2, lymphatic nodules in the mucous membrane; 3, submucosa; 4, muscularis; 5, mesentery of the 
appendix; 6, pus and fibrin covering the appendix; 7, dense infiltration of the wall of the appendix 
with pus. 

3. At one or more points in the wall of the appendix there is an 
exudative inflammation with necrosis. In this way small or large 
portions of the wall of the appendix are destroyed, large or small 
perforations are formed, and the contents of the appendix escape into 
the abdominal cavity. In these cases the appendix usually contains 
a fsecal concretion. Such perforations are regularly followed by the 
formation of an abscess around the appendix (Fig. 283). The pus 
may extend from this abscess in any direction and for long distances, 
so that we find abscesses deep in the pelvic cavity, or under the 
diaphragm, or at other remote points. 



THE ALIMENTARY CANAL. 575 

4. The entire appendix becomes gangrenous within one or two 
days, with the formation of an abscess, or general peritonitis. This 
is the most fatal form of appendicitis; its etiology is obscure. 

5. In catarrhal or croupous colitis the inflammation may extend to 
the appendix. 

6. In typhoid fever there may be changes in the wall of the ap- 
pendix of a character similar to those in the wall of the small intes- 
tine. 

7. There may be a tuberculous inflammation of the appendix, 
with the formation of ulcers. 

As the result of chronic inflammation in the appendix strictures 
or obliteration of the lumen of the appendix may occur. 

The lumen of the appendix frequently contains concretions of fsecal 
material which have often been mistaken for foreign bodies. For- 
eign bodies, such as grape and apple seeds, and various small objects 
which have been swallowed, sometimes, though rarely, find their way 
into the appendix. Both the fsecal concretions and the foreign bodies 
may act as important predisposing agents of inflammation and per- 
foration of the appendix, through pressure, erosion, etc., of the 
mucous membrane, affording portals of entry to various forms of 
pathogenic micro-organisms. 

The Streptococcus pyogenes, Staphylococcus pyogenes, the Ba- 
cillus coli communis, and Bacillus proteus are the bacteria most 
commonly found associated with the lesions of acute appendicitis and 
its accompanjing peritonitis. 1 

TUMORS. 

Myomata. — Tumors composed of smooth muscle and connective 
tissue grow in the muscular coat and project inward. They may be 
large enough to obstruct the intestine, and may then give rise to 
intussusception. In the duodenum such tumors may obstruct the 
common bile duct. Less frequently these tumors project outward 
into the peritoneal cavity. 

Lipomata may be developed from the submucous coat and grow 
inward, or from the subserous coat and project outward into the peri- 
toneal cavity. 

Polypoid Tumors, projecting into the cavity of the intestine and 
composed of connective tissue and covered with epithelium, are fre- 
quently found. They are associated with catarrhal inflammation or 

1 Bodenpyl, "Etiology of Appendicitis, " New York Medical Journal, December 
30th, 1893. Consult also, Kelynack, "The Pathology of the Vermiform Appendix, ' : 
1893. Berry, Jour. -of Path, and Bact., vol. in., p. 160, 1895 (bibliography). 
Mibbert, Virch. Arch., Bd. cxxxii., p. 66. 



576 THE ALIMENTARY CANAL. 

occur by themselves. They are found throughout the intestinal tract 
and may be single or multiple. They grow from the submucous coat 
and project inward. Some of them are small, solid, connective-tissue 
tumors, covered by the mucous membrane which they have pushed 
inward. Others are of the same character, but of large size. In 
others the connective tissue is arranged in branching tufts, covered 
with cylindrical epithelium ; and in these last tumors there may also, 
be tubules lined with cylindrical epithelium, giving to the growth 
the characters of an adenoma. 

Adenomata are found in the duodenum and colon. They form 
flat infiltrations of the wall of the intestine, or project inward as poly- 
poid tumors. They are composed of tubular follicles, like those of 
the intestinal mucous membrane, and of a connective-tissue stroma. 
In some of these tumors the tubules have a tolerably regular shape 
and arrangement; there is no infiltration of surrounding tissue; the 
tumor is of benign nature. In other tumors the tubules are irregular 
in shape and arrangement, and the growth infiltrates the surrounding 
parts. There is no sharp dividing line between these tumors and the 
carcinomata. 

Carcinomata are found in the colon and the duodenum, and are 
of three varieties. 

1. The new growth is composed of tubules lined with cylindrical 
epithelium. It begins as a flat infiltration of the submucous coat, 
which soon surrounds the intestine, infiltrates the whole thickness of 
the wall of the gut, and may extend to the surrounding soft parts. 
Fungous masses project into the cavity of the intestine, while at the 
same time ulcerative and destructive processes are going on. Ac- 
cording to the exact arrangement of the growth, there is more or less 
stenosis of the intestine. 

2. The growth has the characters of colloid cancer and forms a 
diffuse infiltration of the intestinal wall, completely surrounding it. 
and often extending over a length of several inches. 

3. In the rectum there is sometimes a carcinomatous growth, 
with flat epithelial cells (epithelioma), like similar growths in the 
skin . 1 

Lymphoma. — Tumors composed of tissue resembling that of the 
lymphatic glands originate in the solitary and agminated nodules, and 
in the intestinal wall in cases of leukaemia and pseudo-leuksemia. 

Similar tumors are found as an idiopathic lesion both in the large 
and small intestines. These tumors are irregular, diffuse growths 
infiltrating the wall of the intestine, the mesentery, and the neigh- 
boring lymph nodules, and reaching a considerable size. They often 

1 Consult Bohm, Virch. Arch., Bd. cxl., p. 524 (bibliography). 



THE ALIMENTARY CANAL. 577 

ulcerate internally and produce dilatation or stenosis of the intes- 
tine. It is hard to tell whether some of these tumors should be called 
lymphomata or sarcomata. 1 

CONCRETIONS (ENTEROLITHS) , 

There are sometimes found in the intestines round, oval, or irreg- 
ular masses of firm consistence. They are usually small, but may 
reach the size of a man's fist. They are composed of faecal matter, 
mucus, bile, the carbonate and phosphate of lime, and triple phos- 
phate. They may produce inflammation, ulceration, and perfora- 
tion. 

FALSE DIVERTICULA OF THE INTESTINE. 

Not infrequently one finds at autopsies either in the small or 
large intestine diverticula or herniae, consisting of the mucous mem- 
brane which has been crowded through the muscularis and is covered 
by the serosa, which project from the exterior of the gut usually near 
its mesenteric attachment. These so-called " false diverticula" may 
be large, but are usually not larger than a pea; they may be single 
or numerous. They usually cause no functional disturbance, but 
may, through the accumulation of faecal material within them, be 
the seat of perforation. 2 

ANTHRAX INTESTINALIS (MYCOSIS INTESTINALIS) . 

The anthrax bacillus may find lodgment in the intestinal mucous 
membrane either by the ingestion of food containing the germ or by 
metastasis through the blood from some other seat of infection, 
especially the skin. 

The intestinal lesions are most apt to occur in the small intestines 
and in the upper part of the colon. 

The mucous membrane is studded with larger and smaller brown 
or black frequently elevated patches, or areas of local congestion, or 
haemorrhage, or necrosis. The mucous membrane near the inflam- 
matory and necrotic foci may be cedematous. Hyperplasia of the 
spleen and lymph nodes is apt to accompany the intestinal anthrax. 
The anthrax bacillus may be found about the seat of local lesion in 
the intestine, in the associated lymph nodes, and when secondary to 
local infection elsewhere it may be found in the primary lesion and 
in the blood. It is believed that other forms of bacteria may cause 

J For study of congenital tumors of the intestines consult Huetes, Ziegler's 
Beitr. z. path. Anat., Bd. xix., p. 391, 1896. 

2 Consult Edel, Yirch. Arch., Bd. cxxxviii., p. 347; also Hanseman, ibid., Bd. 
cxliv., p. 400. 
46 



578 THE ALIMENTARY CANAL. 

intestinal lesions somewhat similar to those of anthrax, but the 
researches in this direction are not yet sufficiently numerous to per- 
mit of very definite statements. 

Ascaris lumbricoides is found in the small intestine, either singly 
or in considerable numbers. In rare cases a number of worms may 
form a mass which produces inflammation, ulceration, and perfora- 
tion. 

Oxyuris vermicularis is found in large numbers in the rectum. 

Tricocephalus dispar is found in the caecum, 

Ankylostomum duodenale is found in the duodenum and may 
give rise to considerable haemorrhages. 

Trichina spiralis is found in its adult condition in the small in- 
testine. 

Pentastomum denticulatum occurs in the submucous tissue of 
the small intestine in an encapsulated condition. 

Cysticercus cellulosce has been seen, in a few cases, on the mu- 
cous membrane. 

Tcenia solium, Taenia mediocanellata, and Bothriocephalus 
latus are all found in the small intestine. 

Very large numbers of various forms of bacteria are regularly 
found in the intestinal cavity, intermingled with its contents and 
clinging to its walls. Among the most common of these is the 
Bacillus coli communis (see page 260). 

THE PERITONEUM. 

The free surface of the parietal peritoneum is covered with a single 
layer of flat, polygonal, nucleated cells. Beneath these cells are succes- 
sive planes of connective tissue extending down to the muscles and 
fasciae. These planes are formed of a fibrillated basement substance 
reinforced by elastic fibres, and of branching cells. Embedded in the 
connective tissue are the nerves, blood vessels, and lymphatics. The 
lymphatic system is very extensive. 

The omentum consists of fibrillated connective tissue arranged so 
as to form a mesh work. The trabecular of the meshwork are com- 
pletely covered by large, flat cells. In the basement substance, be- 
neath the endothelium, are branching cells. In the larger trabecular 
are blood vessels, lymphatics, and fat. Sometimes we find on the 
larger trabecular little nodules formed of polygonal or branched cells. 

MALFORMATIONS. 

Arrest of development of the peritoneum occurs in the shape of 
fissures in the mesial line or external to it ; in the case of the dia- 
phragm being absent, of a fusion with the pleura ; and as defective 



THE ALIMENTARY CANAL. 5?9 

development of the mesentery, the omentum, and the other folds of 
the peritoneum. 

Excess of development occurs in the shape of unusual length of 
the mesentery, the omentum, and the other folds of the peritoneum ; 
or of supernumerary folds and pouches. These are chiefly found in 
the hypogastric, iliac, and inguinal regions and near the fundus of 
the bladder. There is access to these sacs by a well-defined fissure or 
ring, which is frequently surrounded by a tendinous band lying in 
the duplicature. They may give rise to internal incarceration of the 
intestines. 

INFLAMMATION. 

The very great extent of the peritoneum, and the readiness with 
which its lymphatic system absorbs foreign matters from the perito- 
neal cavity, render peritonitis a most severe and dangerous form of 
inflammation. 

If the greater part of the peritoneum is inflamed we call the lesion 
a general peritonitis. If only a circumscribed area is involved it is 
a local peritonitis. The course of the inflammation may be rapid or 
slow, so that we speak of acute and chronic inflammation. The 
inflammation may be attended with the production of tubercle tissue, 
and then it is a tubercular peritonitis. 

I. Acute Peritonitis. 

The acute inflammations of the peritoneum may occur as idio- 
pathic lesions without discoverable cause ; but much more frequently 
they are directly due to some appreciable cause. 

Wounds and contusions of the wall of the abdomen ; wounds, ulcers, 
new growths, incarcerations, intussusceptions, ruptures, perforations, 
and inflammations of the stomach and intestines ; inflammation of the 
vermiform appendix ; injuries, ruptures, and inflammations of the 
uterus, ovaries, and Fallopian tubes ; rupture and inflammation of 
the bladder ; inflammation of and about the kidneys ; abscesses and 
hydatid cysts of the liver ; inflammation of the gall bladder and 
large bile ducts ; thrombosis of the portal vein ; inflammations of the 
spleen, pancreas, lymphatic glands, retroperitoneal connective tissue, 
vertebrse, ribs, and pelvic bones ; septicaemia and the infectious dis- 
eases, and chronic Bright's disease — are all ordinary causes of acute 
peritonitis. 

According to the exact cause of the inflammation, the peritonitis 
is at first either local or general. A local peritonitis may remain cir- 
cumscribed, or it may spread and become general. 

We can distinguish two anatomical forms of acute peritonitis. 

1. Cellular Peritonitis. — This form of peritonitis may be pro- 
duced by any irritant which does not act too energetically. It can be 



580 



THE ALIMENTARY CANAL. 



excited in dogs by injections of very small quantities of a solution of 
chloride of zinc. In the human subject we find it with perityphlitis,, 
with circumscribed abscesses in the peritoneal cavity, and in cases 
of puerperal fever which die within forty-eight hours after the devel- 
opment of symptoms. 

After death we find the entire peritoneum of a bright-red color 
from the congestion of the blood vessels ; but there are no fibrin, no 
s erum, no pus, no other lesions visible to the naked eye. Minute 
examination, however, shows a very marked change in the endo- 




Fio. 284.— Acute Cellular Peritonitis. 
Human omentum, X 750 and reduced. 

thelial cells. They are increased in size and number, and the new 
cells coat the surface of the peritoneum and project outward in little 
masses (Fig. 284). 

2. Exudative Peritonitis. — The ordinary form of acute perito- 
nitis is attended with the production of serum, fibrin, and pus, and 
with changes in the endothelium and connective-tissue cells. 

If we inject a solution of chloride of zinc or of some other irri- 
tant into the peritoneal cavity of a dog, we find that by the end of 
one or two hours inflammatory changes are evident. There is a lit- 
tle serum in the peritoneal cavity, a general congestion of the peri- 



THE ALIMENTARY CANAL. 581 

toneum, and little knobs and threads of fibrin on its surface. There 
are no marked changes in the endothelium or connective- tissue cells, 
but pus cells are present, in moderate numbers in the stroma just be- 
neath the endothelium, and white blood cells in the vessels. 

After the lapse of twenty-four hours the lesions are more marked. 
The congestion of the peritoneum is much more decided, there is 
more serum in its cavity and a thicker layer of fibrin and pus on its 
surface. Minute examination shows that two distinct sets of chan- 
ges are going on at the same time : (1) a production of fibrin, se- 
rum, and pus ; (2) a swelling and multiplication of the endothelial 
cells. If the inflammation is very intense the pus and fibrin are 
most abundant ; if the inflammation is milder the changes in the 
endothelium are more marked. The fibrin coagulates on the free 
surface of the peritoneum. The white blood cells collect in large 
numbers in the blood vessels, and as pus cells infiltrate the stroma 
and collect on its surface. There is no special change in the con- 
nective-tissue cells. The endothelial cells may remain in place, 
although their edges and corners are separated by pus cells and knobs 
of fibrin ; or the endothelium falls off in large patches ; or the sur- 
face of the peritoneum is covered with numerous cells which look 
like endothelial cells more or less deformed. But few dogs survive 
the third day of an acute artificial peritonitis. 

In the human subject, if death takes place before the third day, 
both the gross and minute changes are the same as those seen in 
the dog. There are present the same general congestion, the pus, 
fibrin, and serum, the desquamation and multiplication of the endo- 
thelial cells (Fig. 285). 

In many cases of peritonitis, however, death occurs between the 
sixth and fourteenth days of the disease. The appearance of the 
peritoneum at this period of the inflammation is not always the 
same. The congestion of the blood vessels may persist, it may be 
very intense and accompanied with extravasations of blood, or it 
may be entirely absent. There may be a thin coating of fibrin and 
pus gluing together neighboring surfaces of peritoneum, or this layer 
may be very thick. The accumulation of pus may be superficial, or 
it may infiltrate the whole thickness of the peritoneum and the sub- 
peritoneal connective tissue. The quantity of purulent serum in the 
peritoneal cavity may be small or large, and this serum may contain 
few or many pus cells, or the serum may be of a dirty -brown color 
and filled with bacteria. When the purulent serum is shut in by 
adhesion it is often thick and yellow, like the pus of an abscess. 

The minute appearances differ from those seen at an earlier stage, 
chiefly in the larger amount of inflammatory products and in the 
changes in the fixed connective- tissue cells. During the first three 



582 



THE ALIMENTARY CANAL. 



days of an acute peritonitis the connective-tissue cells are but little 
changed, but by the seventh day there is a marked increase in their 
size and number. 

Acute peritonitis may prove fatal by the fourteenth day ; or it 
may be succeeded by chronic peritonitis ; or the patients recover and 
permanent connective-tissue adhesions and thickenings of the peri- 
toneum are left behind. Recovery is most common when the peri- 
tonitis has been a local one. 

Many species of bacteria have been found in the exudate in acute 
exudative peritonitis, but the significance of many of them is very 







/4Hr£fr*. 






Fig. 285.— Acute Exudative Peritonitis, eight days 1 duration. 
Human omentum, x 850 and reduced. 

uncertain on account of the liability to contamination of the exudate, 
either before or after death, by the germs in the intestinal contents. 

Streptococcus pyogenes, Bacillus coli communis, Staphylococcus 
pyogenes, Micrococcus lanceolatus, Bacillus pyocyaneus, Bacillus 
aerogenes capsulatus, and many others have been reported. The Strep- 
tococcus and the Bacillus coli communis appear to be most frequently 
present. Very often two or more micro-organisms are associated in 
the exudate. 



Consult Taml and Lanz, "Peritonitis, "Mitth. a. Kl. u. Med. Inst. d. Schweiz, 
1 Reihe, Heft i., p. 1, 1893 ; also Silberschmidt, ibid., Heft 5, p. 432. 



THE ALIMENTARY CAXAL. 



583 



The probability of the passage of bacteria without visible perfor- 
ation through the intestinal wall should be borne in mind. 1 

II. Chronic Peritonitis. 

We find the following varieties of chronic peritonitis : 
1. Cellular Peritonitis. — This form of peritonitis is found as a 
complication of chronic endocarditis, of cirrhosis of the liver, of 
chronic pulmonary phthisis, and of acute general tuberculosis. 

Neither fibrin nor pus is present, but there may be clear serum in 
the peritoneal cavity. The peritoneum may look normal to the naked 
eye, or it may be studded with very minute, translucent nodules. 




Fie. 286.— Chronic Cellular Peritonitis occurring with Pulmonary Phthisis. 
Human omentum, x 750 and reduced. 



Minute examination shows changes in the endothelial cells and 
the connective-tissue cells. These cells are everywhere increased in 
number and altered in shape ; or, to speak more guardedly, the sur- 
face of the peritoneum is covered with, cells which look as if they 
were derived from the endothelium and the connective-tissue cells 
(Fig. 286). Some are large, flat cells ; some smaller, polygonal 
cells ; some irregularly fusiform ; some large, granular masses con- 

*Arnd, ibid., Heft 4, p. 395. 



584 THE ALIMENTARY CANAL. 

taining a number of nuclei. Although these new cells are found 
over most of the surface of the peritoneum, yet they are more nu- 
merous in little patches which are scattered here and there. 

2. Peritonitis with Adhesions. — There may be a formation of 
permanent adhesions without the production of fibrin or pus. It is 
often, indeed, difficult to tell whether old peritoneal adhesions are due 
to the form of chronic peritonitis of which we are now speaking, or 
whether they are the result of an acute peritonitis. But there are 
some cases in which the mode of development of the adhesions seems 
evident. 

If, from perityphlitis or some other cause, a collection of pus is 
shut in in some part of the peritoneal cavity, we may find the rest of 
the peritoneum smooth and shining ; no serum, fibrin, or pus, no 
thickening ; but the neighboring surfaces of the peritoneum are at- 
tached to each other by adhesions. These adhesions are in the shape 
of threads and membranes, often of the most extreme tenuity. They 
are formed of a fibrillated basement substance, the fibrils crossing 
each other in all directions. In the basement substance are cells, 
some fusiform and stellate, but most of them look like large branch- 
ing cells, of which the cell bodies have become fused with the base- 
ment substance while the nuclei remain. 

Close to these adhesions the peritoneum may appear normal to the 
naked eye, but if it is put in water very fine threads and membranes 
will float upward from its free surface. Minute examination shows 
that the connective-tissue cells are increased in size and number, that 
the endothelial cells are replaced by cells of a great variety of shapes, 
and that the thin little threads and membranes on the surface are 
formed of large branching cells (Fig. 287). 

Such a peritonitis with adhesions appears to be a more advanced 
stage of the cellular peritonitis just described, but the inflammation, 
instead of stopping at the production of cells alone, goes on to the 
formation of membranes. 

We sometimes find in the same patient chronic pleurisy with adhe- 
sions and chronic peritonitis with adhesions. 

3. Chronic Peritonitis with Thickening of the Peritoneum. — 
This form of peritonitis occurs quite frequently as an idiopathic 
lesion. It may involve the greater part of the peritoneum or be con- 
fined to the capsules of the liver and spleen. 

The most marked feature of the lesion is the thickening of the peri- 
toneum — a thickening which may reach as much as an inch. The 
outer portions of the thickened peritoneum are composed of dense 
connective tissue, the inner layers of granulation tissue. The surface 
of the peritoneum is smooth or covered with fibrin. There may also 



THE ALIMENTARY CANAL. 



585 



be connective-tissue adhesions between different parts of the perito- 
neum. The peritoneal cavity contains clear and purulent serum. 

In some cases the parietal peritoneum is principally involved ; in 
others the peritoneum of the stomach, intestines, liver, and spleen. 
The thickening of the capsule of the liver is attended with a diminu- 
tion in the size of that viscus. 

4. Chronic Peritonitis with the Production of Fibrin,, Serum, 
and Pus. — This form of peritonitis may follow acute peritonitis, may 
be due to lesions of the abdominal viscera, or may occur without 
known cause. 

The abdominal cavity contains purulent serum, either free or shut 





! 




Fig. 287.— Chronic Peritonitis with Adhesions, x ?50 and reduced. 
Parietal peritoneum. 

in by adhesions. The surface of the peritoneum is coated with fibrin 
and connective-tissue adhesions. The coils of intestine, and all the 
neighboring surfaces of the peritoneum, are matted together partly 
by fibrin, partly by permanent adhesions. 

5. Hcemorrhagic Peritonitis. — This occurs most frequently as a 
local inflammation. It involves the peritoneum behind and around 
the uterus in the female, and that covering the recto-vesical excava- 
tion in the male. The affected portion of the peritoneum is covered 



586 THE ALIMENTARY CANAL. 

with layers of new membrane infiltrated with blood. The membranes 
are formed of connective tissue containing numerous blood vessels 
and infiltrated with blood. The extravasations of blood may form 
tumors of considerable size. 

General hsemorrhagic peritonitis is described by Friedreich. In 
two cases of ascites, which had been frequently tapped, he found the 
visceral and parietal peritoneum covered with a continuous mem- 
brane of a diffuse yellowish-brown color, mottled with extravasations 
of blood. The membrane was thickest over the anterior abdominal 
wall. It could be separated into a number of layers. These layers 
were composed of blood vessels, masses of pigment, branching cells, 
and fibrillated basement substance. In many places the extra vasated 
blood was coagulated in the shape of round, hard, black nodules. 
The entire new membrane could be readily stripped off from the 
peritoneum. 

6. Tuberculous Peritonitis. — This occurs as one of the lesions of 
acute general tuberculosis, with chronic pulmonary phthisis, with 
tuberculous inflammation of the genito-urinary tract, and as a local 
inflammation. 

The gross appearance of the lesion varies. 

When tuberculous peritonitis occurs as one of the lesions of general 
tuberculosis, there are numerous small miliary tubercles, increase in 
the size and number of the endothelial and connective- tissue cells, and 
sometimes a little fibrin. Some of the miliary tubercles are com- 
posed of tubercle tissue, others of round and polygonal cells. 

As a complication of tuberculosis of the genito-urinary tract we 
find the peritoneum studded with miliary tubercles, coated with fibrin, 
and serum is also present in the peritoneal cavity. 

As a complication of chronic phthisis there are miliary tubercles 
in the peritoneum of the small intestine immediately over the tuber- 
cular ulcers of the mucous membrane. There may also be thickening 
of the peritoneum and permanent adhesions. 

The anatomical forms of primary tuberculous peritonitis are: 

1. The peritoneum is everywhere studded with miliary tubercles, 
its surface is coated with a thin layer of fibrin. 

2. The peritoneum is studded with miliary tubercles, or with 
larger cheesy nodules; in its cavity are large quantities of serum. 

3. The peritoneum is studded with miliary tubercles or with 
cheesy nodules. Its cavity contains large quantities of fibrin, which 
not only coat the peritoneum but fill up the spaces between the 
viscera. 

4. In addition to the presence of miliary tubercles in the perito- 



THE ALIMENTARY CANAL. 587 

neum its apposed surfaces are fastened together by connective-tissue 
adhesions. The coils of small intestine especially are fastened to- 
gether in this way. 

5. The tuberculous inflammation is confined to the omentum. By 
the formation of tubercle tissue and of connective tissue the omentum 
is converted into a hard tumor, which occupies the upper part of the 
abdominal cavity. 

6. There are miliary tubercles in the peritoneum, connective- 
tissue adhesions, and collections of serum and pus. In this way the 
abdominal cavity becomes divided up into cavities of different sizes, 
each cavity containing more or less serum and pus. 

TUMORS. 

Fibromata are developed from the subperitoneal connective tis- 
sue and project inward into the peritoneal cavity. They are found 
beneath the parietal peritoneum and that covering the intestines. 
Such tumors may reach a very considerable size. Papillary fibromata 
of the peritoneum may be secondary to papillary fibroma of the 
ovary. 

Lipomata. — Circumscribed tumors composed of fat tissue are 
formed beneath the intestinal and parietal peritoneum and in the 
mesentery. These tumors may become changed into fibrous tissue 
or calcified. Their pedicles may become atrophied so that they are 
left free in the peritoneal cavity. 

When they grow beneath the parietal peritoneum they may form 
fat hernise. At the umbilicus, in the inguinal canal, along the vas 
deferens, in the crural ring, and in the foramen obturatorium, fatty 
tumors may grow, project outward under the skin like herniae, and, 
by drawing the peritoneum after them into a pouch, may open the 
way for a future intestinal hernia. 

Plexiform Angio- Sarcoma. — Very large tumors, resembling in 
their gross appearance colloid cancer, have been described by Wal- 
deyer. 1 They are formed by a new growth of blood vessels, with a 
production of gelatinous tissue from their adventitia. 

Carcinoma of the peritoneum is either secondary or primary. 
The primary tumors assume the character of colloid cancer or of 
common cancer. 

The colloid form frequently involves the greater part of the peri- 
toneum and forms a large mass which distends the abdomen. The 
omentum is changed into a large, gelatinous mass; the subjacent 
muscles, the lymphatic glands, and the liver are infiltrated with the 
new growth, and soft, gelatinous masses project into the peritoneal 

1 Virch. Arch., Bd. lv., p. 134. 



588 THE ALIMENTARY CANAL. 

cavity. The umbilicus is sometimes invaded, so as to project out- 
ward in the form of a semi-translucent tumor. The appearance of 
the new growth is that of a soft, jelly-like mass embedded in a 
fibrous stroma. The minute structure is that of a connective-tissue 




Fig. 288.— Cystic Papilloma of the Omentum. 
Secondary to papilloma of the ovaries (Freeborn). 



stroma, arranged so as to form cavities of different sizes. These 
cavities are filled with a homogeneous, gelatinous basement substance 
and with polygonal cells. 

Common carcinoma appears in the form of numerous small 



THE ALIMENTARY CANAL. 589 

nodules scattered everywhere in the inner layers of the peritoneum. 
These nodules are small, firm, and white, and are composed of a 
fibrous stroma enclosing cavities filled with polygonal cells. With 
the formation of these nodules there are often associated a general 
thickening of the peritoneum, an accumulation of serum in the peri- 
toneal cavity, and adhesions. 

Sarcomata appear in the form of solitary, slowly growing tumors 
behind the peritoneum or between the folds of the mesentery. 

These retroperitoneal sarcomata are found both in children and 
adults. They usually originate behind the peritoneum covering the 
posterior part of the abdominal wall. 

The retroperitoneal sarcomata may be of the small spheroidal- 
celled type (lympho-sarcoma) or of the fusiform-celled type. They 
are often very vascular. At first they grow slowly inward, pushing 
forward the peritoneum and abdominal viscera. After a time they 
assume a more noxious character, infiltrating the soft parts with 
which they come in contact, and forming metastatic tumors in 
the omentum, mesentery, intestinal wall, liver, lungs, and in other 
viscera. 

Endotheliomata similar in structure to those originating in the 
pleura are of occasional occurrence in the peritoneum. They may 
form single well-defined tumors or flattened masses in the thickened 
peritoneum. 

Cuboidal or polyhedral cell masses often grouped along the 
side of anastomosing channels in the new-formed or old connective- 
tissue stroma sometimes lend a glandular character to the type of 
growth. 1 

Cysts of the mesentery are of occasional occurrence. They may 
be filled with chyle, with blood, or with serous fluid, 2 or may be due 
to the echinococcus. Lipomata of the mesentery are recorded. 

Multiple cysts of the omentum may form by transplantation of 
papillary cyst-adenomata from the ovary (see Fig. 288). 

PARASITES. 

Echinococci can be formed in their regular way at any part of 
the visceral and parietal peritoneum, or be free in the peritoneal 
cavity. These cysts may be small, or so large as nearly to fill the 
abdominal cavity. 

Cysticercus cellulosce may also be developed in the subperitoneal 
connective tissue. 

1 See Endothelioma, p. 312. 

2 Regarding cysts of the mesentery consult Weichselbaum, Virchow's Archiv, 
Bd. lxiv., p. 145; Bramann, Archiv fur klin. Chirurgie, Bd. xxxv., p. 201; Hahn, 
Berliner klin. Wochenschrift, June 6th, 1887, p. 408 ; Robinson, British Medical 
Journal, January 31st, 1891. 



THE LIVER 



MALFORMATIONS. 

Congenital malformations of the liver are not common and are 
of little practical importance. The organ may be entirely wanting ; 
the lobes may be diminished or increased in number ; its form may be 
altered, so that it is rounded, flattened, triangular, or quadrangular. 
The gall bladder or gall ducts may be wanting ; the ductus choledo- 
chus may be double, both ducts emptying into the duodenum, or one 
emptying into the duodenum, the other into the stomach. The single 
ductus choledochus may also empty into the stomach. Owing to 
abnormal openings in the diaphragm or the abdominal parietes, the 
liver may suffer displacement upward or forward. In congenital 
transposition of the viscera the liver is found on the left side, the 
stomach and spleen on the right side. 

Small, isolated bodies, having the same structure as the liver, have 
been a few times found in the suspensory ligament and in the lesser 
omentum. 

ACQUIRED CHANGES IN SIZE AND POSITION. 

As a result of tight lacing very marked changes are sometimes 
produced in the shape of the liver. By the narrowing of the base of 
the thorax the organ is compressed from side to side, and its convex 
surface is pressed against the ribs. In consequence of this there are 
found ridges and furrows on its convex surface. In consequence also 
of the circular constriction, a part of the right, and usually of the left 
lobe also, becomes separated by a depression. Over this depressed 
and thinned portion of the liver the capsule is thick and opaque. In 
extreme cases the depressing and thinning reach such an extent that 
there is only a loose, ligamentous connection between the separated 
portion and the liver. 

A series of depressions are sometimes found on the upper surface 
of the right lobe of the liver, running from front to back, apparently 
caused by folds of the organ. 

Structural changes in the liver may induce changes in its size and 
shape. It may be increased in size by tumors, hydatid cysts, abscesses, 



THE LIVER. 591 

fatty and amyloid degeneration, by congestion, and sometimes by 
cirrhosis, etc. 

It may be diminished in size by atrophy, by cirrhosis, by acute 
parenchymatous degeneration, etc. 

Changes in the position of the liver are produced by alterations in 
its size, by pressure downward from the thoracic cavity and upward 
from the abdomen, by the constriction of tight lacing, by tumors or 
circumscribed serous exudation between the liver and diaphragm, by 
curvature of the spine. 

The liver is readily turned, by pressure from above or below, on 
its transverse axis. The transverse colon may be fixed above the 
liver so as to push it backward, downward, and to the right. There 
are a few cases recorded of dislocated and movable livers. These 
occurred in women who had borne children and whose abdominal walls 
were lax. "With ascites it is not uncommon to find the liver quite 
movable. 1 

ANEMIA AND HYPEREMIA. 

Ancemia of the liver may be general or partial. It may be due to 
general anaemia or to local disturbances of the circulation, such as 
swelling of the cells in parenchymatous or other degeneration, pres- 
sure of tumors, etc. The organ appears pale, often of slightly yellow- 
ish or brownish color. It may be harder than usual, and smaller. 

Hypercemia of the liver is either an active or a passive process. 
In health the amount of blood in the liver varies at different times, 
being regularly increased during the process of digestion. When the 
digestive process is unduly influenced by the ingestion of spirits, 
spices, etc. , the hyperemia assumes abnormal proportions, and when 
this is often repeated it may lead to structural changes in the organ. 
Severe contusions over the region of the liver sometimes cause a hyper- 
emia, which may result in suppurative or in indurative inflammation. 
In hot climates and in malarious districts active and chronic hyper- 
emia of the liver are frequent and often cause structural lesions. 
In scurvy, also, the liver is sometimes congested. Cessation and 
suppression of the menses and of hemorrhoidal bleeding may cause 
hyperemia of the liver. In all these varieties of active congestion 
the liver is enlarged, of a deep-red color, and blood flows freely from 
its cut surface. 

The passive congestions of the liver are produced by some obstruc- 
tion to the current of blood in the hepatic veins. Valvular diseases 
of the heart, emphysema and fibrous induration of the lungs, large 
pleuritic effusions, intrathoracic tumors, angular curvature of the 
spine, aortic aneurisms pressing on the vena cava, and constrictions 

Consult Graham, "Displacements of the Liver, "Trans. Assn. Am. Phys., vol 
x. , p. 258, 1895 (bibliography) . 



592 THE LIVER. 

of the vena cava and of the hepatic veins, may all produce a chronic 
hypersemia of the liver. In all these cases, as the congestion affects 
principally the hepatic veins, we find the centre of each acinus con- 
gested and red while its periphery is lighter in color. This gives to 
the liver a mottled or nutmeg appearance {nutmeg liver). The liver 
cells in the centre of each acinus are frequently colored by little gran- 
ules of red or black pigment, and the cells at the periphery become 
fatty, so that the nutmeg appearance is still more pronounced. A 
liver in this condition is usually of medium size, but may be smaller 
or larger than normal. 



ritibN 









fin- 






^3 




xM^M'ti^ 






:^&*|5i^b* 



-s"vi: 



Fig. 2S9.— Chronic Congestion of the Liver (nutmeg liver). 
This section shows complete atrophy of the liver cells at the centre of the lobule, a, dilated 
vena centralis; b, dilated capillaries filled with blood; c, portal vein surrounded by connective tis- 
sue; d, gall duct; e, atrophied liver cells; g, nearly normal liver tissue. 

When the congestion is long-continued the veins at the centre of 
each acinus may become permanently dilated, the hepatic cells in 
their meshes become atrophied (Fig. 289), so that the centre of each 
acinus consists only of dilated capillaries or of these and new connec- 
tive tissue ; or the dilatation and atrophy of the liver cells may, in 
circumscribed portions of the organ, involve the entire acinus. In 
long-continued congestion the liver is usually smaller than normal, 
and may be slightly roughened or uneven on the surface ; but it is 



THE LIVER. 593 

sometimes enlarged. The peculiar nutmeg appearance may be very 
well marked, or it may not be evident, the organ being of a dark-red 
color. 

WOUNDS, RUPTURE, AND HEMORRHAGE. 

Wounds of the liver may induce haemorrhage, which, if life con- 
tinue, is followed by inflammation. Serious wounds of the liver are 
usually fatal, but recovery may occur -even after the destruction of a 
considerable portion of the organ. 

Rupture of the liver may be produced by severe direct contusions 
or by falls. It may be produced in children by artificial delivery. 
The rupture usually involves both the capsule and a more or less con- 
siderable portion of the liver tissue. It is commonly accompanied by 
large haemorrhage, and is usually fatal. 

Hcemorrhage. — Extravasations of blood in the substance of the 
liver, or more frequently beneath the capsule, are found in new-born 
children after tedious or forcible labors. In adults haemorrhage, 
except as the result of injury, is uncommon. Extravasations of 
blood are sometimes seen in malignant malarial fevers, especially in 
tropical climates ; in scurvy, purpura, and phosphorus poisoning ; 
and bleeding may occur in and about soft tumors, abscesses, and 
echinococcus cysts. It may also occur as a result of thrombosis of 
the hepatic vein. 

LESIONS OF THE HEPATIC ARTERY. 

The hepatic artery is in rare cases the seat of aneurisms which 
may attain a large size. Such aneurisms may displace the liver tis- 
sue, compress the bile ducts so as to cause jaundice, and may rupture 
into the stomach or abdomen. 

Owing to its abundant anastomoses, emboli of the branches of the 
hepatic artery usually induce no marked lesions, out they sometimes 
result in haemorrhagic infarctions. 

LESIONS OF THE PORTAL VEIN. 

Thrombosis, Embolism, and Inflammation. — Thrombosis of the 
branches of the portal vein may be produced by weakening of the cir- 
culation from general debility — marasmatic thrombi; by pressure 
on the vessel from without, as in cirrhosis, tumors, gall stones, dila- 
tation of the bile ducts, etc. ; by injury ; by the presence of foreign 
materials within the vessel ; and as a result of inflammation of its 
wall, or of embolus. The thrombus may form in the vessels in the 
liver or be propagated into them from without. It may partially or 
47 



594 THE LIVER. 

entirely occlude them. The clot may become organized as a result of 
endophlebitis, and a permanent occlusion of the vessel ensue. If the 
clot be a simple, non-irritating one, leading to occlusion, the conse- 
quences are usually more marked in the abdominal viscera than in 
the liver itself. The branches of the hepatic artery form sufficient 
anastomoses to nourish the liver tissue and prevent its necrosis, even 
in complete occlusion of the portal vein ; and if occlusion occur slow-, 
ly the organ may continue to perform its functions. But this oblite- 
rative form of thrombosis is usually attended by ascites, enlargement 
of the spleen, dilatation of the abdominal veins, and sometimes by 
haemorrhage from the stomach and intestines. 

In another class of cases, in addition to the local and mechanical 
effects of a thrombus, there may be necrotic changes and suppurative 
inflammation in the walls of the vessels or in the liver tissue about 
them. The thrombi are apt to soften and break down, and the frag- 
ments may be disseminated through the smaller trunks of the portal 
vein. In this way, by the distribution through the smaller vessels 
of a disintegrated thrombus from a large trunk, or by the introduc- 
tion into the branches of the portal vein of purulent or septic material 
from some of the abdominal viscera or from wounds, multiple foci of 
purulent inflammation in the portal vein, and multiple abscesses in- 
volving the liver tissue, may be produced. In many cases the pre- 
sence of bacteria may be detected in the inflammatory foci. 

These soft thrombi of the portal vein and the accompanying pyle- 
phlebitis and abscess may be caused in a variety of ways. Ulcera- 
tion of the intestines and stomach, abscesses of the spleen, suppurative 
inflammation of the mesentery and mesenteric glands, inflammation 
and ulceration of the bile ducts from gall stones, inflammation of the 
umbilical vein in infants, may all induce thrombi in their respective 
veins, which may be propagated to the portal vein or may give rise 
to purulent or septic emboli. Two cases are recorded in which a fish 
bone in the portal vein induced suppurative inflammation in that 
vessel. One of these cases, occurring in Bellevue Hospital in 1867, was 
reported by Dr. E. G. Janeway. Male, 47 ; dying, after a four weeks' 
illness, in a typhoid condition, with lesions of sero-flbrinous peritoni- 
tis and chronic diffuse nephritis. There were numerous small ab- 
scesses in the right lobe of the liver, two in the left lobe. The left 
division of the portal vein contained a firm red and white clot over 
an inch long ; the right division was lined with a firm thrombus. 
The walls of the vein were thickened and contained purulent fluid. 
A fish bone, two inches long, its centre covered by a thrombus, lay 
half in the mesenteric and half in the portal vein. 

In infants inflammation of the umbilical vein may not only induce 
inflammation of the portal vein and abscesses in the liver, but multiple 



THE LIVER. 595 

abscesses in various parts of the body, and acute peritonitis may be 
induced. 

Rupture of the Portal Vein, with fatty degeneration of its 
walls, has occurred in a few instances. 

Chronic Endophlebitis, with atheroma and calcification, may 
occur in the walls of the portal vein, giving rise to thrombosis. 

Dilatation of the Portal Vein, either uniform or varicose, may 
occur in various parts of the vessel or its branches. It may be caused 
by destruction of the liver capillaries in cirrhosis, or by occlusion of 
the vein by thrombi, tumors, etc. 

THE HEPATIC VEINS. 

The hepatic veins present lesions similar to those of the portal vein 
and its branches, but they are much less frequent. They may be 
dilated by obstruction to the passage of venous blood into the heart. 
They may be the seat of acute and chronic inflammation, and soft 
thrombi and suppurative inflammation may be produced by abscesses 
in the liver. 

ATROPHY OF THE LIVER. 

Atrophy of the liver may affect the entire organ or be confined to 
some part of it. General atrophy may occur in old age as a senile 
change, or may be induced by starvation or chronic exhausting dis- 
eases. The organ is diminished in size, is usually firm, and the acini 
appear smaller than usual. Microscopically the change is seen to be 
due to a diminution in size of the liver cells, and hand-in-hand with 
this there occurs frequently an accumulation of pigment granules 
within the atrophied cells. The cells may entirely disappear over 
circumscribed areas, leaving only shrivelled blood vessels and con- 
nective tissue ; or, in some cases, there may be an increase of con- 
nective tissue in connection with the atrophy of the cells. When 
much pigment is formed in the cells the lesion is often called pigment 
atrophy. 

Essentially the same changes may occur in circumscribed portions 
of the liver, as the result of pressure from new connective tissue in 
cirrhosis, from tumors, hydatids, amyloid degeneration, gall stones, 
etc. In atrophy from pressure the liver cells are apt to become very 
much flattened and squeezed together as they diminish in size. 

DEGENERATIVE CHANGES. 

Acute Degeneration ; Parenchymatous Degeneration (Cloudy 
Swelling). — In a variety of acute and infectious diseases — pneumo- 
nia, typhoid and typhus fevers, scarlatina, variola, diphtheria, ery- 
sipelas, yellow fever, septicaemia, and in certain cases of acute anas- 



596 THE LIVER. 

mia and phosphorus poisoning — the liver is somewhat swollen and, 
on section, of a dull yellowish-gray color, looking somewhat as if it 
had been boiled. It contains less blood than usual, and the outlines 
of the lobules are indistinct. Microscopical examination shows the 
lesion to consist of a swelling of the liver cells and an accumulation 
in them of moderately refractile, finer and coarser albuminous gran- 
ules. Those granules may disappear and the cells return to their 
normal condition, or, as is frequently the case, they may pass into 
a condition of fatty degeneration. Very frequently fatty and paren- 
chymatous degenerations are associated together. 

Small areas of necrosis of liver cells may be found in certain 
acute infectious diseases (see Fig. 07). 

Fatty Infiltration. — In the normal human liver there is usually 
a certain amount of fat in the liver cells, and this amount varies con- 
siderably under different conditions. 

The gross appearance of pathological fatty livers varies a good 
deal, depending upon the amount and distribution of fat and its as- 
sociation with other changes. If the lesion is uncomplicated and 
considerable the organ is increased in size, the edges rounded, the 
consistence firm, the color yellowish, and the cut surface greasy. 
The lobules are enlarged and their outlines usually indistinct, and 
the blood content diminished. The liver is increased in weight. If 
the amount of infiltration be moderate the outlines of the lobules 
may be more distinct than usual and the centres appear unusually 
red. This is due to the fact that the accumulation of fat usually 
commences in the periphery of the lobules and progresses toward 
the centre, so that the centre appears darker by contrast with the 
fatty periphery. The lesion may be uniform throughout the organ 
or it may occur in patches. In the latter case the liver has a mot- 
tled appearance, irregular yellowish patches alternating with the 
brownish-red, unaffected portions. 

Fatty infiltration is often associated with chronic congestion {nut- 
meg liver), with cirrhosis and amyloid degeneration ; the picture 
may then present considerable complexity. Fatty livers may be 
stained brown or greenish with bile pigment. 

Microscopically the liver cells are seen to contain larger and 
smaller droplets of fat (Fig. 290), and frequently large drops of fat 
occupy nearly the entire volume of the cell, so that the protoplasm 
may be visible only as a narrow, nucleated crescent at one side, or 
it may disappear altogether (Fig. 291). The microscopical appear- 
ances of course vary, depending upon the degree of infiltration and 
the association with other lesions. 

Fatty infiltration of the liver may occur as a result of excessive 
ingestion of oleaginous food ; in chronic alcohol, phosphorus, and 



THE LIVER. 



597 



arsenic poisoning ; in certain exhausting diseases accompanied by 
malnutrition, as in pulmonary phthisis, chronic dysentery, etc. ; and 
under a variety of conditions which we do not understand. 

Fatty Degeneration. — In this condition, which in many cases 
cannot be morphologically distinguished from fatty infiltration, the 
fat is believed to be formed by a transformation of the protoplasm 




Fig. 290.— Fatty Infiltration op Liver Cells. 



of the liver cells. The fat droplets are, for the most part, very 
small and abundant, though this is not constant. Fatty degenera- 







•V J * « «.i 



'r\ 



mm* 



n. 



i»^r~^\^ ,V..' -V 



W^yh X?AKi?^A 



v4\* 






5^? /^ \®r ^'/ «$^ y <-">-- ~. «*- ^" o 






Fig. 291.— Fatty Infiltration of Liver. 
Portion of the periphery of a lobule. 



tion of the liver cells frequently follows, and is associated with, 
cloudy swelling under the varying conditions in which this occurs, 
or it may appear in profound anaemia and in acute phosphorus and 
arsenic poisoning. 

Amyloid Degeneration (Waxy Liver).— In the liver amyloid 
degeneration may be general or local ; so extensive as to give the 



508 



THE LIVER. 



organ very characteristic appearances, or so slight as to be unrecog- 
nizable without the aid of the microscope. It may be associated 
with other lesions. When the change is extensive and general the 
liver is enlarged sometimes to more than twice its normal size ; the 
edges are thickened and rounded ; the surface smooth ; the tissue 
tough, firm, inelastic, more or less translucent, and of a brownish- 
yellow color. The lobular structure may be more or less indistinct, 
or it may become very evident by an associated fatty degeneration 
of the peripheral or central cells of the lobules. The translucency 
and peculiar appearance of the tissue may be best seen by slicing off 
a thin section and holding it up to the light. When the lesion is 




c 





I 




S 



c 



Fig. 292.— Amyloid Degeneration of the Liver. 
The degenerated walls of the vessels are stained red. 



less considerable the liver may be of the usual size, and may feel 
harder than normal, and here and there a translucent mottling may 
be evident, or the degeneration may be apparent only on the addi- 
tion of staining agents. When, as is frequently the case, it is as- 
sociated with cirrhosis, the liver may be small and nodular, and the 
appearance of the cut surface will vary greatly, depending upon the 
character of the cirrhotic change and the presence or absence of fat. 
This degeneration usually commences in the walls of the intra- 
lobular blood vessels, causing them to become thickened and translu- 
cent. The liver cells are squeezed by the thickening of the vessels 
and may become partially or completely atrophied (Fig. 292). 



THE LIVER. 599 

It is stated by some observers that the liver cells may also become 
waxy, but we have been unable to find them unmistakably thus 
changed. The liver cells not infrequently undergo fatty metamor- 
phosis. Amyloid degeneration may also involve the interlobular ves- 
sels, and in advanced stages larger and smaller areas of liver tissue 
may be nearly or completely converted into the dense, refractile sub- 
stance which in its arrangement but obscurely represents the group- 
ing and structure of the affected lobules. Xot infrequently atrophic 
or fatty liver cells are seen scattered singly or in clusters through the 
amyloid masses. In the affected regions the blood content of the 
liver is considerably diminished, or it may be nearly entirely absent. 

Amyloid degeneration of the liver is usually associated with a 
similar lesion of other organs, such as spleen, kidneys, intestines, etc.. 
although it may occur in this organ alone. It usually occurs in 
cachectic conditions, as in chronic phthisis : in chronic suppurations, 
especially of the bones ; in syphilis, and sometimes in malarial poison- 




W 



Fig. 293.— Pigijestatiok of the Liver ex vEaearlax Fever. 
The pigment in this specimen was contained in cells lying within the liver capillaries. 

ing. It occasionally occurs unassociated with any of these con- 
ditions. 

PIGMENTATION OF THE LIVER. 

As a result of severe malarial poisoning a variable amount of 
brown, black, or reddish pigment is often found in the blood. This is 
usually mostly taken up by the leucocytes and deposited in various 
parts of the body, chiefly in the liver, spleen, and marrow of the 
bones. In the liver it is usually found enclosed in variously shaped 
cells which lie especially in the blood vessels, but sometimes in the 
tissue between them (see Fig. 293). The liver cells frequently con- 
tain bile pigment, but usually are free from the melanotic pigment 
characteristic of this malarial condition. As the result of this ac- 
cumulation of pigment the liver may have a dark reddish-brown, an 
olive-brown, or black color (sometimes called bronze liver). This 
condition may be associated with various other lesions of the liver, 
depending upon the nature and extent of which the organ will present 



600 THE LIVER. 

a great variety of appearances. Thus there may be fatty or waxy 
degeneration, cirrhosis, chronic congestion, etc. 

Pigment may be found in the connective tissue along the portal 
vessels similar in character to that which occurs in the lungs from 
the inhalation of coal dust. This inhaled pigment, according to the 
researches of Weigert, doubtless finds access to the blood and is de- 
posited in the liver as it is in the spleen and hepatic lymph nodes. 

Pigmentation of the liver cells, which is to a certain extent nor- 
mal, may be greatly increased as a result of atrophy, localized haemor- 
rhage, and of obstructive jaundice. 1 

ACUTE YELLOW ATROPHY OF THE LIVER. 

This disease is characterized anatomically by a rapid diminution 
in the size of the liver as the result of a granular and fatty degenera- 
tion and disintegration of the liver cells. The liver, sometimes with- 
in a few days, may be reduced to one-half its normal size. On open- 
ing the abdominal cavity the organ may be found lying, concealed 
by the diaphragm, close against the vertebral column. The amount 
of diminution and the general appearance of the affected organ de- 
pend to a considerable extent upon its previous condition — i.e., 
whether or not it was the seat of other lesions — as well as upon the 
degree of degenerative change. In general, if the lesion is well 
marked, the liver is small, flabby — sometimes almost fluctuating — 
and the capsule wrinkled. On section the cut surface may show but 
little trace of lobular structure, but presents an irregular mottling 
with gray, ochre-yellow, or red ; sometimes one, sometimes another 
color preponderating. 

Microscopical examination shows varying degrees of degeneration 
and destruction of the liver cells. Most evidently in those parts which 
have a grayish appearance, the outlines of the cells are preserved 
and the protoplasm is filled with larger and smaller granules. In 
the yellow portions the outlines of the liver cells may be preserved, 
and they may contain varying quantities of larger and smaller fat 
droplets and granules of yellow pigment. Or the cells may be com- 
pletely disintegrated, and in their place irregular collections of fat 
droplets, pigment granules, red and yellow crystals, and detritus ; 
only the connective tissue and blood vessels of the original liver tis- 
sue remaining. The red areas may show nearly complete absence of 
liver cells and cell detritus, and sometimes irregular rows of cells 
which are variously interpreted as being new-formed gall ducts or 
proliferated liver cells. In these areas it appears to be, in part at 

1 The distribution and amount of the pigment may be well seen by staining thin 
sections with eosin and mounting in eosin-glycerin or balsam. 



THE LIVER. 601 

least, the blood contained in the vessels which imparts the red color. 
Sometimes the interstitial tissue is infiltrated with small spheroidal 
cells resembling leucocytes. Crystals of leucin and tyrosin are 
sometimes found intermingled with the cell detritus. In some cases 
the liver is not diminished in size. 

These lesions of the liver are frequently associated with enlarge- 
ment of the spleen and parenchymatous degeneration of the kid- 
ney and of the heart muscle. Multiple haemorrhages may occur in 
the gastro-intestinal canal, kidneys, bladder, and lungs. There is 
usually marked jaundice. Rod-shaped bacteria and micrococci have 
been found in the liver, but their significance is doubtful : we have 
not been able to find them in the cases which we have examined. 
The cause of the disease is unknown, and it is doubtful whether it is 
a disease primarily of the liver or an acute infectious disease with 
local lesions. It is not unlikely that more than one form of lesion is 
grouped under this heading. 1 

INFLAMMATION OF THE LIVER, 

Acute Hepatitis (Purulent Hepatitis : Abscess of the Liver). — 
Purulent or suppurative inflammation of the liver may be the result 
of injury : it may be secondary to inflammation of the gall ducts or 
the branches of the portal vein. It may occur as the result of the 
presence of tumors, parasites, or from propagation of an inflam- 
matory process from without, as in ulcer of the stomach with ad- 
nesions to the liver and secondary involvement of the latter. It is 
often directly due to the introduction into the organ, through the 
blood vessels or gall ducts or otherwise, of bacteria. Purulent in- 
flammation in the liver almost always results in abscess. 

Large abscesses of the liver may be traumatic, but are often due 
to unknown causes. The\ are not infrequently associated with dys- 
entery, and may then be due to the conveyance of micro-organisms 
through the veins, or lymph channels, or peritoneum, or gall ducts from 
the intestinal ulcers. They may be due to the presence of the amoeba 
coli. They occur most frequently in tropical climates, but are not 
very uncommon in the temperate zone. They are usually single, 
but there may be several of them. They are sometimes so large as 
to occupy a large part of the lobe. They are most frequent in the 
right lobe, but may occur in any part of the organ. They tend to 
enlarge, and as they do so they approach the surface of the liver. 
Here the contents of the abscess may be discharged into the perito- 



1 For an account of a bacterial study of a case of Infectious Febrile Icterus 
(Weil"s disease') consult Jaeger. Zeits. f. Hvgiene u. Infectkr., Bd. xli. 3 p. 525 
1892. 

48 



602 THE LIVER. 

neal cavity. More frequently, however, as they approach the sur- 
face, a localized adhesive peritonitis ensues, so that the liver becomes 
bound to adjacent parts, and thus the abscess may open into the 
pleural cavity, or, owing to a secondary pleurisy with adhesions, into 
the lung tissue. They may open into the pericardium. They may 
open externally through the abdominal wall ; into the stomach, duo- 
denum, colon, or pelvis of the right kidney ; into the hepatic veins, 
portal vein, vena cava, or gall bladder or gall ducts. 

The early stages in the formation of large abscesses of the liver 
are but little known. It is probable, however, that in many cases 
they are the result of the confluence of smaller abscesses. Their 
contents, usually bad smelling, may be thick and yellow like ordi- 
nary pus, but more commonly they are thin, reddish-brown, or green- 
ish in color from admixture with the pus of blood, gall pigment, and 
broken-down liver tissue. Microscopical examination shows the con- 
tents to consist of fluid with pus cells, more or less degenerated blood, 
degenerated liver cells, fragments of blood vessels, and pigment 
granules and crystals. The walls of the abscess are usually ragged, 
shreds of necrotic liver tissue hanging from the sides. Microscopical 
examination of the liver tissue near the abscess shows infiltration with 
pus, flattening of the liver cells from pressure, cloudy swelling, and 
necrosis of those lying along the cavity. Bacteria or the amoeba coli 
or both may be present. Liver abscesses due to the presence of the 
amoeba coli have certain peculiarities, concerning which reference is 
made to the studies of Councilman and Lafleur, " Amoebic Dysen- 
tery," Johns Hopkins Hospital Reports, vol. ii., p. 490, 1892. 

The amoebic abscesses are usually free from bacteria. Other ab- 
scesses may contain the Bacillus coli communis, or the Streptococcus 
pyogenes or Staphylococcus pyogenes. 

Not infrequently, however, especially in old abscesses, examination 
both morphological and cultural fails to reveal the presence of micro- 
organisms. 

After the discharge of the contents of the abscess or without this 
if it be not very large, granulation tissue may form in the wall of the 
cavity and a fibrous capsule be produced, enclosing the contents, 
which become thickened and often calcareous, and in this condition 
may remain for a long time. Or the connective-tissue walls may 
approach one another and join, forming a fibrous cicatrix at the seat 
of the abscess. 

Several large abscesses may, one after another, heal in this way 
after evacuation of their contents, with little diminution in the size 
of the liver. 1 

1 Edebohls, " Dysentery and Hepatic Abscess with Amoeba Coli, " Proceedings of 
the New York Pathological Society, 1892. 



THE LIVER. 603 

Abscesses of the liver accompanying inflammation of the portal 
vein and gall duct are considered elsewhere in this section. 

Small multiple metastatic abscesses are not infrequent in pyse- 
mia, and are called pycemic abscesses. In these abscesses we can 
readily study the various stages of formation. Suppurative processes 
in any part of the body — in the head, upper and lower extremities, 
etc. — may act as distributing centres for micro-organisms. 1 These, 
entering the circulation, may pass the heart and pulmonary capil- 
laries, with or without inducing lesions in the lungs, and, lodging 
in the vessels of the liver, induce circumscribed necrosis of the liver 



M 





s &.■:- 


»v - 










tf~ 


W.'.'S 








j'*»^ «. "^ 




C &'OAh 


, C V» 












*1 l«i 


.$ V- 




'"'A', " 




-":; ""^"^v 










v v 


'•« 




^ 







."; 



& 



•'-^3- ';..■ <*"?•■ 



TJms 



Fig. 294.— Small Abscesses in the Liver containing Bacilli. 
Associated with a suppurative inflammation of the gall bladder and gall ducts. 

tissue (see Fig. 294) and suppurative inflammation. Under these 
conditions we may find on a section of the liver larger and smaller 
yellowish or grayish spots, the larger of which may be soft and pre- 
sent the usual characters of abscesses. The smaller, which may not 
be larger than a pin's head, may present the usual consistence of 
liver tissue with the lobular structure still evident; others may be 
softer, more yellow, and surrounded by a zone of hypersBmic liver tis- 
sue. Microscopical examination of the earlier stages often shows the 
blood vessels filled with micrococci, scattered and in masses. Around 
1 Kruse and Pasqnale, Zeits. f . Hygiene u. Infkr. , Bd. xvi. 



604 



THE LIVER. 



these the liver cells are found in various stages of necrosis ; in many 
the nuclei do not stain and the bodies are very granular, or the entire 
cell is broken down into a mass of detritus. About these necrotic 
islets of liver cells pus cells collect and often form a zone of dense 
infiltration. Thus, by the increase of pus cells and the necrosis of 
liver tissue, small abscesses are formed whose contents are inter- 
mingled with greater or less numbers of bacteria, which seem to in- 
crease in number as the process goes on. By the confluence of small 



fi ■ 




—Or 






Fig. 295.— Chronic Interstitial Hepatitis. 
a, new-formed connective tissue; b, dilated blood vessels of the new tissue; c, gall duct; 
d, parenchyma of liver. 

abscesses larger ones may be formed. Death usually ensues, how- 
ever, before the abscesses attain a very large size. 

Chronic Interstitial Hepatitis (Cirrhosis). — The most marked 
result of chronic interstitial hepatitis is the formation of new connec- 
tive tissue in the liver. The character, amount, and distribution of 
the new tissue vary greatly in different cases. Secondarily there are 
usually marked changes in the liver cells and in the blood vessels and 
gall ducts. The new tissue is most commonly formed and most 



THE LIVER. 605 

abundant in the periphery of the lobules along the so-called capsule 
of Glisson, but it may extend into the lobules between the liver cells. 
It may surround single lobules, or more frequently larger and smaller 
groups of lobules (Fig. 295). It may occur in broad or narrow, ir- 
regular streaks or bands. It is frequently more abundant in one part 
of the liver than in another. The new-formed tissue tends to con- 
tract, and thus compromise by pressure the enclosed islets of liver 
tissue, causing them to project, in larger and smaller nodules, from 
the surface of the organ. The liver cells may be flattened or atro- 
phied from pressure; or, from interference with the portal circula- 
tion, they may atrophy or become fatty; or they may become colored 
with bile pigment. The varied appearances with cirrhotic livers 
present to the naked eye depend largely upon the amount and distri- 



/< 















■#^>; 







Fig. 296.— Hypertrophic Cirrhosis of the Liver. 
Showing formation of connective tissue between the liver cells. 

bution of the new connective tissue and upon the secondary changes 
in the liver cells. 

In some cases the liver is enlarged, sometimes so much so as to 
weigh nine or ten pounds, the surface smooth or slightly roughened 
— hypertrophic cirrhosis : in other cases it may be finely or coarsely 
nodular on the surface. It may be smaller than normal, sometimes 
very small indeed, so as to weigh only one or two pounds — atrophic 
cirrhosis. The surface may then be very rough and uneven from 
the projection of larger and smaller nodules of liver tissue, or it may 
be quite smooth; or the organ may be greatly distorted by the con- 
traction of large bands or masses of new connective tissue. In sec- 
tion through cirrhotic livers the new tissue may not be visible to the 
naked eye, or it may appear as grayish, irregular streaks, or bands, 
or patches, often sharply outlined against the dark-red, or brown, or 



606 



THE LIVER. 



yellow, or greenish-yellow parenchyma. When, as is often the case, 
fatty infiltration is associated with atrophic cirrhosis the liver, may 
not only not be diminished in size but may be larger than normal. 

On microscopical examination the new connective tissue is found 
in some cases loose in texture and containing many variously shaped 
cells; or it may be dense and contain comparatively few cells; it is 
usually quite vascular. In some forms of hypertrophic cirrhosis 
there may be a very general and extensive growth of new fibrous tis- 
sue in and along the capillaries between the liver cells (Fig. 296) . 
In other cases of hypertrophic cirrhosis the new growth of connective 




2r&Aj 



mS^^^0^^M 




Fig. 297.— Chronic Interstitial Hepatitis. 
Showing a portion of the section shown in Fig. 244, but more highly magnified, a, portions of 
liver lobules; 6, new-formed connective tissue; c, gall ducts, apparently new formed; d, blood 
vessels in the new tissue. 

tissue is abundant between the liver lobules and along the smaller 
gall ducts, without encroaching materially upon the parenchyma. 
Not infrequently, when occurring largely between the lobules, it will 
be found to have encroached more or less upon their peripheral por- 
tions. Very frequently there are found in the new connective tissue 
cylindrical ducts lined with cuboidal cells, and resembling gall ducts 
(Fig. 297, c) ; or irregular rows of more or less cuboidal or polyhedral 
cells, which look somewhat like the lining cells of the medium-sized 
gall ducts, or like altered liver cells. The branches of the hepatic 



THE LIVER. 60? 

and portal veins, particularly the latter, often become obliterated by 
pressure from the new connective tissue or from chronic thickening 
of their walls, so as to seriously interfere with the functions and 
nutrition of the liver cells. The bile ducts also may become obliter- 
ated, or there may be catarrhal inflammation, especially of the larger 
trunks. The branches of the hepatic artery are much less liable to 
alterations than the other vessels. The capsule of the liver is usually 
thickened, either uniformly or in irregular patches; or its surface 
may be roughened by larger and smaller papillary projections. The 
liver is frequently bound to the diaphragm or other adjacent organs 
by connective-tissue adhesions. Amyloid and fatty degeneration 
may be associated with cirrhosis. Cirrhotic livers frequently show 
an unusual number of leucocytes in the blood vessels. 

The obstruction to the portal circulation induced by cirrhosis 
usually gives rise to a number of secondary lesions, since collateral 
circulation is rarely established in sufficient degree to afford much 
relief. The- hsemorrhoidal and vesical veins may be greatly enlarged, 
and also veins of communication between Glisson^s capsule and the 
diaphragmatic veins. 

In rare cases a very peculiar dilatation of the cutaneous veins 
about the umbilicus is observed. The enlarged veins form a circular 
network around the umbilicus, or a pyramidal tumor alongside of it, 
or all the veins of the abdominal wall, from the epigastrium to the 
inguinal region, are dilated. This condition is said to be produced 
by the congenital non-closure and subsequent dilatation of the umbil- 
ical vein and its anastomoses with the internal mammary, epigastric, 
and cutaneous veins. According to Sappey, it is not the umbilical 
vein which is dilated, but a vein which accompanies the ligamentum 
teres. 

There is very frequently also a dilatation of the veins of the 
abdominal wall, which has a different cause. It is produced by the 
pressure of the fluid of ascites on the vena cava, and is found with 
ascites from any cause and with abdominal tumors. 

Ascites is the most common secondary lesion of cirrhosis. It 
usually begins at an early stage of the disease, and is apt to increase 
constantly. It usually precedes oedema of the feet, but both may 
appear at the same time. This fluid is of a clear yellow or brown, 
green or red ; it is sometimes mixed with shreds of fibrin, and more 
rarely with blood. The peritoneum remains normal, or becomes 
opaque and thick, or there may be adhesions between the viscera. 

The spleen is very frequently enlarged, and the enlargement may 
be very considerable. When it is not increased in size this seems 
usually due to previous atrophy of the organ, or to fibrous thickening 



608 THE LIVER. 

of its capsule, or to haemorrhages from the stomach and bowels occur- 
ring just before death. 

The stomach and intestines are often secondarily affected by the 
obstruction to the portal circulation. Profuse haemorrhage from the 
stomach and intestines may occur and sometimes cause sudden death. 
The mucous membrane is then found pale, or congested, or with 
hsemorrhagic erosions. Sometimes the blood is infiltrated in the 
coats of the stomach and intestines. The mucous membrane of the 
stomach, and of the entire length of the intestines, is frequently the 
seat of chronic catarrhal inflammation, and is sometimes uniformly 
and intensely congested and coated with mucus. In other cases both 
the mucous and muscular coats are pale, but very markedly thickened. 

Cirrhosis of the liver is not infrequently accompanied by chronic 
diffuse nephritis. 

The causes of cirrhosis are imperf ecly understood. It is a disease 
of adult life, but exceptionally occurs in children. In adults it seems 
in many cases to be directly dependent upon the continued ingestion 
of large quantities of strong alcoholic liquors. It very rarely occurs 
as a result of beer drinking. There are many cases of cirrhosis for 
which no cause can be discovered. It is probable that in certain cases 
a degeneration of circumscribed areas of liver parenchyma precedes 
and probably determines the new formation of connective tissue. 
Welch ' has described the occurrence of small circumscribed areas of 
fibrous tissue in the liver, replacing liver cells and containing coal 
pigment. This rare lesion he has called cirrhosis hepatis anthra- 
cotica. 

Syphilitic Hepatitis. — Chronic interstitial inflammation of the 
liver very frequently results from syphilitic infection, either congeni- 
tally or in the later stages of the acquired form. It may occur in a 
diffuse manner, new connective tissue being formed either between 
the lobules, or within them between the rows of liver cells. The new 
tissue may be rich in cells, or dense and firm. This form is fre- 
quently seen in children, and cannot be distinguished, either macro- 
scopically or microscopically, from similar forms of interstitial he- 
patitis from other causes. 

In other cases, particularly in children, there may be numerous 
small gummata (so-called miliary gummata) scattered through the 
liver, together with more or less new connective tissue (Fig. 298). In 
adults gummata are usually larger, varying in size from that of a 
pea to a hen's egg, and may be surrounded by larger and smaller 
irregular zones of ordinary connective tissue (Fig. 299). In still 

1 Welch, V Cirrhosis hepatis anthracotica," Johns Hopkins Hospital Bulletin, Febru- 
ary and March, 1891. 



THE LIVER. 609 

other cases in adults we find larger and smaller dense, irregular 
bands or masses of connective tissue running through the liver, 
drawing in the capsule and often causing great deformity of the 
organ. These bands and masses of new tissue may or may not en- 
close gummata, either large or small. These deforming cicatrices, 
either with or without gummata, are very characteristic of syphilitic 
inflammation of the liver. 

This, like the simple interstitial inflammation of the liver, may be 

r\ nam fc '- 3EHH :i\^\ ^ «■ 



j» 



3C1 



Fig 298 —Syphilitic Hepatitis. 
A so-called miliary gumma from the liver of a child with congenital syphilis. 

associated with fatty and waxy degeneration, and with atrophy of 
the parenchyma from pressure. 

Tuberculous Hepatitis. — This lesion, which is usually secondary 
to tubercular inflammation in some other part of the body, or a part 
of acute general miliary tuberculosis, is most frequently characterized 
by the formation of larger and smaller miliary tubercles, which may 
be either within or between the liver lobules or in the walls of the 
bile ducts. Many of the tubercles are too small to be seen with the 
naked eye ; others may be just visible as grayish points ; still others 
may be from one to three mm. in diameter, with distinct yellowish- 
white centres. Microscopical examination shows considerable varia- 
49 



610 



THE LIVER. 



tion in the structure of the tubercles in different cases, as well as in 
the same liver. Some of them, usually the smaller ones, consist 
simply of more or less circumscribed collections of small spheroidal 
cells, which are not morphologically distinguishable, so far as the 
form and arrangement of the cells are concerned, from simple inflam- 
matory foci, or from the diffuse masses of lymphatic tissue which 
occur normally in the liver. 

In other forms we find a well-marked reticulum with, larger and 
smaller spheroidal and polyhedral cells, with or without giant cells. 
In still other forms there is more or less extensive cheesy degenera- 
tion. The larger forms are conglomerate, being composed of several 
tubercle granula joined together to form a single nodular mass. The 




v; $& 



Fig. 299.— Gumma op Liver. 



a, cheesy centre; b fibrous periphery; c, small-celled peripheral infiltration; d, portions of live 
lobules. 

liver cells at the seat of the tubercle are destroyed, and the interstitial 
tissue and blood vessels either destroyed or merged into the tubercle 
tissue. In the periphery of the tubercles the liver cells may be in a 
condition of coagulation necrosis, and the tissue round about may be 
infiltrated with small spheroidal cells. There is in some cases a new 
formation of gall ducts or of structures which resemble these, and 
which in transverse sections look considerably like giant cells. Tu- 
bercle bacilli, frequently in small numbers, but often in great abun- 
dance, may be found within the tubercles. 

Tuberculosis of the liver may be associated with cirrhosis, waxy 
and fatty degeneration. 

Much more rarely than the above form there are found in the liver 



THE LIVER. 611 

more or less numerous scattered tubercular masses from the size of a 
pea to that of a walnut or larger, with cheesy centres and usually a 
new growth of connective tissue in the periphery. These so-called 
solitary tubercles of the liver may be softened at the centres. Tu- 
bercular inflammation of the gall ducts may give rise to numerous 
scattered, cheesy nodules, as large as a pea or larger, which may be 
softened at the centre and stained yellow with bile. This lesion is 
rare and seems to be more frequent in -children than in adults. 

Perihepatitis. — Acute inflammation of the serous covering of 
the liver, with the formation of fibrin, may occur as a part of acute 
general or localized peritonitis, and over the surface of abscesses, 
tumors, hydatids, etc. , of the organ, when these lie near or approach 
the surface ; or it may be secondary to acute pleurisy. 

Chronic perihepatitis, resulting in the thickening of and forma- 
tion of new connective tissue in and beneath the capsule of the liver, 
may be secondary to an acute inflammation of the capsule, or it may 
be chronic from the beginning and associated with chronic pleurisy, 
chronic peritonitis, and cirrhosis. In this way more or less exten- 
sive adhesions of the liver to adjacent structures may be formed ; 
or, by contraction of the new-formed connective tissue, consider- 
able deformity of the liver may be produced. The capsule is some- 
times uniformly thickened, sometimes the new tissue occurs in more 
or less sharply circumscribed patches. The surface is sometimes 
roughened from little, irregular projecting masses of connective 
tissue. Microscopically the new-formed tissue is usually dense and 
firm, but it may be loose in texture and contain many cells. Not in- 
frequently bands or masses of connective tissue run inward from 
the thickened capsule between the superficial lobules, causing local- 
ized atrophy of the parenchyma. 

Hyperplasia of Lymphatic Tissue in the Liver. — In some 
forms of leuksemia and pseudo-leuksemia the liver is not infrequently 
enlarged and soft and besprinkled with small white spots, or streaked 
with narrow whitish, irregular bands, or of a diffuse grayish color. 
Microscopical examination shows this change to be due to an accu- 
mulation of cells resembling leucocytes, either along the portal vein, 
■or diffusely through the liver tissue, or in small circumscribed masses. 
The amount of accumulation of these small cells varies much, but is 
sometimes so great as to seriously compromise the liver cells. The 
origin of these new cells is not yet definitely known. They may be* 
and doubtless in part are, brought to the organ through the portal 
vein ; but they may, in part at least, be formed in the liver itself, 
possibly from the capillary endothelium. 

In typhoid fever, small-pox, scarlatina, diphtheria, and measles 
small circumscribed masses of cells resembling leucocytes are some- 



612 THE LIVER. 

times found in the liver, lying in the meshes of a delicate reticular 
tissue. These are sometimes called miliary hjmphomata j but it 
should be remembered that small masses of lymphatic tissue nor- 
mally occur in the liver, and that as, under the above conditions, an 
hyperplasia of the lymph nodes and spleen is wont to occur, these 
so-called lymphomata are very probably normal structures, which 
have become more prominent under the conditions of disease owing, 
to an acute inflammatory condition induced by absorbed ptomaines. 

TUMORS OF THE LIVER. 

Tumors of the liver may be primary or secondary ; the latter are 
most common. 

Cavernous Angiomata. — These tumors, usually small, from five 
to fifteen mm. in diameter, are most common in elderly persons 
and are of no practical significance. They may be situated at the 
surface or embedded in the organ, and are of a dark-red color ; 
sometimes sharply circumscribed by a connective-tissue capsule, 
sometimes merging imperceptibly into the adjacent liver tissue. 
Microscopically they consist of a congeries of irregular cavities (Fig. 
144, page 327) filled with blood and frequently communicating freely 
with one another. The walls of the cavities consist of connective 
tissue, often containing small blood vessels, and are sometimes thick, 
sometimes thin. They are believed to be formed by dilatation of 
the liver capillaries, with subsequent thickening of their walls and 
atrophy of the adjacent liver cells. 

Small fibromata and lipomata have been described, as also fibro- 
neuromata of the sympathetic. 

Adenomata of the liver are of not infrequent occurrence. They 
are sometimes small and circumscribed, sometimes very large and 
multiple. They present two tolerably distinct types of structure. 
In one form the tissue presents essentially the same structure as nor- 
mal liver tissue, except that the arrangement of the cells is less uni- 
form and the cells are apt to be larger. They look like little islets of 
liver tissue, sometimes encapsulated and sometimes not, lying in the 
liver parenchyma. In the other form the cells are less like liver 
cells, are frequently cylindrical, and are arranged in the form of 
irregular masses of tubular structures with more or less well-de- 
fined lumina. These tumors are sometimes large and multiple, and 
in one case described by Greenfield there were metastatic tumors 
in the lungs. These tubular adenomata are in some cases so closely 
similar to some of the carcinomata as to be scarcely distinguishable 
from them, and seem, indeed, to merge into them. Cysts, may de- 
velop in adenomata. 1 



l See Dmochowskt and Janowski, Ziegler's Beitr. z. path. Anat., Bd. xvi., p. 102. 



THE LIVER. 613 

Carcinomata are the most coruroon and important of the liver 
tumors, and may be primary and secondary. Primary carcinomata 
of the liver are probably developed from the epithelium of the gall 
ducts, and in some cases are arranged along the larger trunks. Their 
cells are usually polyhedral, sometimes cylindrical, and may be ar- 
ranged irregularly in alveoli or form more or less well-defined tubular 
structures. 

Secondary carcinomata of the liver, which are by far the most 
common, are most frequently due to the dissemination in the organ 
of tumor cells from carcinomata of the stomach, intestines, pancreas. 
or gall bladder. But they may be the result of metastases from the 
mamma, oesophagus, uterus, and various other parts of the body. 
In secondary carcinomata the cells resemble more or less closely the 
type of those forming the primary tumor. 

The form in which the carcinomatous nodules in the liver present 
themselves is subject to considerable variation. Sometimes they are 
single, but more often multiple ; they may be very large, or so small 
as to be scarcely visible to the naked eye : very frequently numerous 
small nodules are grouped in the periphery of a larger cancerous 
mass. They are sometimes deeply embedded in the liver, sometimes 
they project from the surface. The liver is frequently enlarged, 
sometimes enormously so. The nodules are usually whitish or 
yellowish or pink in color, but they are often the seat of hsemor- 
rhages, and may become softened at the centre, forming cysts filled 
with degenerated tumor tissue which is often mixed with blood. The 
nodules are sometimes hard, sometimes soft and almost diffluent. 
Fatty degeneration is frequent, and may be evident to the naked eye 
in the form of yellowish streaks or patches on the cut surfaces. 
Owing to the degeneration and partial absorption of the central por- 
tions of the tumors, the nodules on the surface frequently present a 
shallow depression at the centre. The tumors may be sharply out- 
lined against the adjacent liver tissue, or may merge imperceptibly 
into it. They may be so large or numerous as to occupy the greater 
part of the enlarged organ. The liver tissue in their vicinity shows 
flattening and atrophy of the liver cells from pressure, and there may 
be infiltration with small spheroidal cells. The tumors may press 
upon the portal vein or its branches, or upon the gall ducts, and thus 
seriously interfere with the functions of the organ. Sometimes, how- 
ever, the tumors are very large and abundant without causing any 
apparent detriment to the liver functions. They are not infrequently 
stained with bile. Melanotic carcinomata sometimes occur in the 
liver, most frequently as secondary tumors. 

In some cases, instead of forming separate, distinct nodules, the 
cancerous growth develops in the form of a diffuse infiltration of the 



614 THE LIVER. 

organ, so that the often greatly enlarged liver is irregularly mottled 
with white and reddish-brown masses, and may then somewhat 
resemble some forms of chronic interstitial hepatitis. 

Sarcomata. — Spindle-celled, melanotic, and telangiectatic sarco- 
mata may occur in the liver as secondary tumors. Secondary myxo- 
mata and chondromata have also been described, but they are very 
rare. Angiosarcoma may occur as a primar} 7 tumor. 1 

Cavernous lymphangiomata have been described in a few cases. 
Cysts, usually of small size, may occur by dilatation of the bile ducts. 
They may be multiple and contain serum, mucus, and degenerated 
epithelium. Single cysts, apparently unconnected with the gall ducts, 
are occasionally found in the connective tissue of the liver. They 
may be lined with ciliated epithelium. 

The liver is sometimes the seat of larger and smaller multiple 
cysts, varying from microscopical size up to that of a pea, and some- 
times larger. They do not appear to communicate with the gall 
ducts. They are sometimes associated with multiple cysts of the 
kidney. Their origin and nature are not understood. 2 

Occasionally the liver is found at the autopsy, even if this be 
made but a few hours after death, more or less completely riddled 
with small, irregular-shaped cavities, from the size of a pin's head to 
that of a pea. These holes are due to the accumulation of gases in 
the liver, and are frequently associated with the presence of the 
Bacillus aerogenes capsulatus (see p. 261). 

PARASITES. 

Echinococcus. — This parasite is the most common and impor- 
tant of those which occur in the human liver. It forms the so-called 
hydatids of the liver. These represent one of the developmental 
stages of the small tapeworm of the dog, Taenia echinococcus 
(see page 108). The cysts in the liver may be very small and multi- 
ple, but they may be as large as a man's head or larger. The liver 
may be greatly increased in size, and the tissue about the cysts 
atrophied. The liver itself furnishes a connective-tissue capsule, 
within which is the translucent, lamellated membrane furnished by 
the parasite. On the inside of this we may find a layer of cells, 
granular matter, and a vascular and muscular system belonging to 
the parasite. Projecting from this inner capsule are the brood cap- 
sules and heads or scolices of the immature tapeworm. The sco- 

1 Arnold, Ziegler's Beitr. z. path. Anat., Bd. viii., p. 123. 

2 Consult Pye- Smith, " Cystic Disease of Liver and both Kidneys," Trans. London 
Path. Soc., vol. xxxii., p. 112, 1881. 



THE LIVER. 615 

lices may become detached from the wall and lie free in the cavity, 
which is filled with a transparent or turbid fluid. Not infrequently 
the cysts are sterile, and are then simply filled with clear or turbid 
fluid ; or the embryos may have died and disintegrated, and their 
detritus, including the hooklets, may be intermingled with the fluid 
contents of the cysts. The contents of the cysts may be mixed with 
fat, cholesterin crystals, pus, bile, or blood; or form a grumous 
mass, in which we may or may not be able to find the hooklets of 
the scolices or fragments of the lamellated wall. The connective 
tissue of the walls of the cysts may be greatly thickened, or they 
may be calcified. 

In other countries the lesion is much more common and fre- 
quently more formidable than in the United States. The cysts 
reach an enormous size, the veins of the liver may be compressed 
and filled with thrombi, the bile ducts compressed and ulcerated. 
So much of the liver tissue may be replaced by the hydatids that 
the patient may die from this cause alone. Very frequently there is 
local peritonitis, and adhesions are formed between the liver and the 
surrounding parts. In some cases the cysts rupture, and their con- 
tents are emptied into the peritoneal cavity, the stomach, the intes- 
tines, the pleural cavity, or the lung tissue. Sometimes the cysts 
perforate the bile ducts, the vena cava, or some of the branches of 
the portal or hepatic veins. Sometimes the abdominal wall is per- 
forated and a fistula formed between the cavity in the liver and the 
surface. 

In cases in which we do not find the scolices entire, a careful ex- 
amination of the inner cyst wall or of its contents will frequently 
establish the diagnosis by revealing single hooklets (see Fig. 40, page 
134) or fragments of the characteristically lamellated wall (see Fig. 
38, page 133). 

Echinococcus multilocularis, which is apparently an abortive 
form of the above species (see page 132), is very rare indeed in the 
United States. The writer (T. M. P.) has examined a specimen 
sent to him by Dr. Edward J. Ill, of Newark, N. J., and which is 
now in the museum of the College of Physicians and Surgeons, 
New York. The patient was a male, age thirty-one, German, sin- 
gle, farmer. He had been in the United States five years. For a 
year previous to his death he had been out of health, and jaundiced 
and somewhat emaciated. A large, indistinctly fluctuating tumor 
was evident in the right lumbar and umbilical regions, and appa- 
rently connected with the liver. Aspiration of the tumor gave a 
milky fluid believed to be pus. An opening was made into the tu- 
mor by one of the surgeons attending the case, and death occurred, 
after ten hours, from haemorrhage. 



616 



THE LIVER. 



The liver was found adherent to the abdominal walls, and about 
one-fourth of the right lobe of the liver was occupied by an irregu- 
lar cavity with very rough, ragged walls. These walls were in 
some places from one to two inches in thickness, and appeared to 
the naked eye to consist of dense connective tissue in irregular 
bands and fascicles, which enclosed very irregular, mostly small 
cavities. Microscopical examination showed that the cavities were 
lined with the delicate, lamellated cuticula characteristic of the echi- 
nococcus cysts. No hooklets were found. Fig. 300 is a drawing 
from this specimen. 




ECHINOCOCCUS MULTILOCULARIS OF THE LlVER. 



Distoma hepaticum, D. sinense, D. lanceolatum, may occur in 
the gall ducts and gall bladder. D. sinense occurs especially in the 
East, and has been found in great numbers in the bodies of China- 
men. D. hcematobium is very common in Egypt and Abyssinia, 
occurring in the blood vessels of the liver. 

Pentastoma denticulatiun is the undeveloped form of Penta- 
stoma taBnioides, a parasite which inhabits the nasal cavity of dogs 
and some other animals. In the liver of man it usually occurs in 
the form of small, rounded, calcified cysts. The cysts may contain 
fat, calcareous matter, and the remains of the dead parasite, among 
which the hooklets may be found. 

Ascaris lumbricoides sometimes finds its way from the intestines 



■^ 



THE LIVER. 617 

into the bile ducts. It may cause no disturbance here, but in some 
cases the worms have been present in large numbers and caused 
occlusion, dilatation, and ulceration of the biliary passages, and have 
led to the formation of abscess of the liver. 

Psorospermia, the very common parasite in the rabbit's liver, 
has been found a few times in the liver of man. 

THE BILIARY PASSAGES. 

Catarrhal Inflammation most frequently attacks the lower por- 
tion of the common duct and the gall bladder. In the acute form 
it usually leaves but few changes appreciable after death. An ab- 
normal coating of mucus, and sometimes congestion of the blood 
vessels^ are almost the only post-mortem lesions. Owing to the 
swelling of the mucous membrane and the accumulation of mucus in 
the lumen, the ducts may be temporarily occluded, but this occlusion 
may not be evident after death. If, however, the inflammation be- 
comes chronic, the walls of the bile ducts may become thickened and 
their lumina more or less permanently obstructed. In consequence 
of this, dilatation or ulceration of the bile ducts may ensue. Tem- 
porary obstruction of the bile ducts may produce marked pigmenta- 
tion of the liver, owing to the accumulation of pigment granules in 
the liver cells, particularly in the vicinity of the capsule of Glisson, 
and jaundice of the entire body. 

The gall bladder may be inflamed by itself — cholecystitis — or in 
connection with inflammation of the biliary passages. If the disease 
is chronic the wall of the bladder may be thickened; polypoid 
growths may occur in the mucosa ; the duct may be occluded ; dila- 
tation, ulceration, the formation of gall stones, calcification, and 
atrophy may ensue. 

Inflammation of the stomach and duodenum, hypersemia and 
inflammation of the liver, concretions, and parasites are the usual 
causes of catarrhal inflammation of the biliary passages, but it may 
occur without these. 

suppuratfve and croupous inflammation of the bile ducts 

(angiocholitis). 

The walls of the ducts may be covered or infiltrated with a fibrin- 
ous or a purulent exudate; they may ulcerate. 

These lesions occur most frequently in connection with obstruc- 
tion of the bile ducts by gall stones or otherwise, and in typhoid and 
typhus fever, pyaemia, cholera, or they may be due to the extension 
of inflammatory processes from without. They also occur under un- 
known conditions. 



618 THE LIVER. 

In many cases of inflammation of the gall ducts, the Bacillus coli 
communis, in fewer, the pyogenic streptococcus and staphylococcus 
are apparently concerned. 

Suppurative inflammation may produce perforations of the ducts 
or bladder, with escape of bile and peritonitis; or fistulous openings 
between the gall bladder and the duodenum, colon, and stomach, or 
through the abdominal wall. Or the inflammation may extend to 
the liver tissue and produce abscesses. Under the latter conditions 
we may find a series of small abscesses ranged along the walls of 
the suppurating gall ducts. In more advanced stages the abscesses 
may become large and communicate with one another, so that a con- 
siderable portion of the liver may be occupied by a series of com- 
municating cavities with ragged walls, containing pus and detritus 
of liver tissue more or less tinged with bile. 

Such abscesses may become more or less completely enclosed by 
conective-tissue walls. The portal vein may also become inflamed, 
and perforations may be formed between it and the bile ducts. 

Constriction and Occlusion may be produced by inflammation 
of the ducts themselves, by new growths in their walls, by calculi or 
parasites in their lumina, by changes in the hepatic tissue in chronic 
and acute hepatitis, by aneurisms, or by pressure on the duct from 
without, as by tumors in the head of the pancreas, etc. 

The obliteration of the smaller bile ducts produces no marked 
lesions. When the ductus communis or the hepatic duct is ob- 
structed, the ducts throughout the liver are frequently dilated and 
the liver tissue bile-stained. The liver may undergo atrophy and 
the whole body be intensely jaundiced. When the cystic duct is ob- 
structed the gall bladder is dilatedo 

Dilatation of the bile ducts is usually produced by strictures in 
the ways just mentioned, or by calculi. When calculi have pro- 
duced the dilatation this condition may sometimes continue after 
they have found their way into the intestines. Sometimes, however, 
we meet with very marked dilatation of the bile ducts without being 
able to make out any present or past obstruction. The dilatation 
may affect only the common and hepatic ducts, or it may extend to 
the smaller ducts in 'the liver, which are then dilated uniformly or 
sacculated. They may contain bile, mucus, or calculi. The liver is 
at first enlarged, but may afterward atrophy. The gall bladder may 
be dilated in consequence of obstruction of the common or the cystic 
duct. In the latter case it may reach an immense size and form a 
large tumor in the abdominal cavity . The dilatation is generally 
uniform, the bladder retaining its normal shape ; sometimes, how- 
ever, there are diverticula, which are usually produced by calculi. 
If the obstruction to the hepatic duct is incomplete or movable the 



THE LIVER. 619 

gall bladder may contain bile, and often calculi. If the obstruction 
is complete the contained fluid may gradually lose its biliary char- 
acter and become a serous or mucous fluid of a light-yellow color — ■ 
hydrops cystidis fellce. The walls of the bladder may be of nor- 
mal thickness, or thinned, or thickened, or calcified. If the obstruc- 
tion is due to a calculus, this may pass into the intestine and the gall 
bladder be suddenly emptied. Usually the bladder fills again, owing 
to its loss of contractile power. 

Biliary Calculi. — These bodies are of common occurrence. They 
are found usually in the gall bladder, sometimes in the hepatic, 
cystic, and common ducts ; less frequently in the small ducts of the 
liver. In the gall bladder from 1 to 7,800 calculi have been counted. 







wsm 






m& *wm 



mm^% 







Fig. 301.— Adenoma of the Gall Duct. 

This section is from a small tumor growing within one of the larger gall ducts within the liver. 
Prepared by Dr. Larkin. 

They vary in size from that of a pin's head to that of a hen's egg, or 
they may be larger. Single gall stones are usually spheroidal or ovoid- 
al ; when multiple they are usually flattened at the sides or faceted. 
They may be composed : 

1. Principally of cholesterin, and may be of pure white color, or 
tinged with various shades of yellow or brown by bile pigment. The 
fractured surface shows a radiating crystalline structure. 

2. Of cholesterin, bile pigment, and salts of calcium and 
magnesium. These are usually dark-colored, brown, reddish-black, 
or green, and may be spheroidal or faceted, smooth or rough on the 
surface ; the fractured surface is usually radiating crystalline. This 
is the most common form. 



620 THE LIVER. 

3. Principally of bile pigment. Such calculi are rare, usually 
small, very dark-colored, and not numerous. 

4. Of calcium carbonate. These are rare, have a nodular surface, 
and a clear crystalline, not radiating fracture. 

Most calculi are formed around a central mass, sometimes called 
the nucleus, which may consist of cholesterin, bile pigment, mucus, 
or epithelium, or more rarely of some foreign body. Thus a dead 
parasite, a needle, and fruit seeds may serve as nuclei. The body of 
the calculus may be homogeneous, or lamellated, or crystalline. 

Biliary calculi in the gall bladder may produce no symptoms and 
only be discovered after death. In the hepatic and common ducts 
they may obstruct the flow of bile and produce fatal jaundice ; or 
they may pass from time to time into the intestine, producing biliary 
colic. If they are impacted in the cystic duct they may produce dila- 
tation of the gall bladder. They may get into the duodenum by 
ulceration through the walls of the ducts or gall bladder, or in the 
same way into the peritoneal cavity. Gall stones which get into the 
intestinal cavity usually pass off without doing any further injury, 
but very large calculi may cause occlusion of the gut with fatal 
results. 

TUMORS OF THE GALL BLADDER AND LARGER GALL DUCTS. 

Small fibromata have been described in the gall bladder and in 
the common duct, but they are very rare. The most common tumors 
are carcinomata. These may be primary or secondary, and present 
the usual structural variations. The cells may be cylindrical, poly- 
hedral, or they may present the characteristics of colloid cancer. 
Primary carcinomata of the gall bladder and larger gall ducts 
are not uncommon. Not infrequently the pancreatic and common 
ducts are both involved, and it is difficult to say whether the tumor 
is primary in the head of the pancreas or in the gall duct. The 
bladder and ducts may also be secondarily involved in carcinomata 
of the stomach, liver, and duonenum. Adenoma of the gall ducts is 
of occasional occurrence (Fig. 301). 



THE SPLEEK 



In studying the alterations produced in the spleen in disease it is 
important to bear in mind the peculiar relations in which this organ 
stands to the blood vessels and to the circulation. After passing 
through the various branches of the splenic artery and the limited 
systems of capillaries which are associated with it, the blood is not 
received at once into venous trunks, as in other parts of the body, 
but is poured directly into the pulp tissue. In this it circulates, un- 
der conditions which render it liable to stagnation and undue accu- 
mulation, before it is taken again into well-defined vessels through 
the open walls of the cavernous veins. Moreover, these conditions 
naturally unfavorable to undisturbed and vigorous circulation, are 
reinforced by the association of the splenic with the sluggish and 
often interrupted portal circulation. Bearing these considerations in 
mind, it will be in a measure plain why, as is in fact the case, the 
spleen should be more liable to alterations in size than any other or- 
gan in the body, and why, serving as it does as a sort of blood filter, 
it should be especially susceptible to the influence of deleterious ma- 
terials of various kinds which in one way or another gain access to 
the blood. In this respect the relations of the spleen to the blood, 
and of the lymph nodes to the lymph, present suggestive analogies. 

WOUNDS, RUPTURE, AND HEMORRHAGE. 

Wounds of the spleen are usually accompanied by extensive 
haemorrhage and are commonly fatal. Death usually occurs as the 
result of this haemorrhage, but it may be due to secondary inflam- 
matory changes. Healing and recovery may, however, occur. 

Rupture of the spleen may be traumatic or spontaneous. In the 
former case it may be due to direct violence in the region of the or- 
gan or to injury to the thorax, falls, etc. In certain diseased condi- 
tions the spleen is more liable to rupture than when it is normal. 
The rupture usually involves not only the capsule, but a more or 
less considerable portion of the parenchyma, and of course leads to 



6*2 



THE SPLEEN. 



hemorrhage. Spontaneous rupture is rare, but may occur as the 
result of excessive enlargement of the organ, as in typhoid fever, 
malaria, etc. — see below — or as the result of abscess. 

Hemorrhage. — Aside from the extensive haemorrhages from in- 
jury and rupture, the spleen may be the seat of small circumscribed 
haemorrhages in various infectious diseases, although, owing to the 
peculiar distribution of the blood, it is often very difficult to distin- 
guish between a moderate interstitial haemorrhage and hyperaemia. 

DISTURBANCES OF THE CIRCULATION. 

Ancemia.— This may be associated with general anaemia, but it 
is not always present in this condition When marked and unasso- 




Fig. 302.— Congestion of the Spleen. 

6, dilated cavernous veins; c, trabeculae of pulp tissue compressed between dilated cavernous 
veins: d, glomerulus. 



ciated with other lesions the spleen is apt to be diminished in size, 
the capsule more or less wrinkled, the cut surface dry and lighter 
in color than normal, the trabeculae unduly prominent. 

In this, as in other alterations simply of the blood content of the 
spleen, neither the gross nor microscopical appearances are constant, 
because of the redistribution of blood which is apt to occur in the 
viscera after death. 

Hypercemia. — This may be passive, occurring when some ob- 
struction to the portal circulation exists, most frequently in cirrho- 
sis of the liver, but also with certain valvular lesions of the heart, 
emphysema, etc. The spleen is enlarged, but usually only to a 
moderate degree. The capsule is apt to be tense, and on section the 



THE SPLEEN. 623 

pulp is dark- red and may be soft or firm. The cavernous veins are 
dilated (see Fig. 302). Usually, when the lesion has existed for 
some time, there is a thickening of the trabeculae and reticular 
framework of the spleen, so that they are prominent on section. In 
other words, there is a chronic interstitial splenitis following the 
chronic congestion. 

Active Congestion of the spleen, which in most cases is scarcely 
to be differentiated from some forms of acute inflammation, and 
probably in many cases is associated with it, very frequently occurs 
in a great variety of acute and infectious diseases, such as typhoid 
fever, pneumonia, diphtheria, pyaemia, the exanthemata, etc. The 
spleen is enlarged, the capsule tense ; on section the pulp is soft, 
dark-red in color, often swelling out from the cut surface and con- 
cealing the glomeruli and trabecules. Under these conditions we 
may find the cavernous veins distended with blood and the inter- 
stices of the pulp infiltrated with a variable, sometimes large quan- 
tity of red and Avhite blood cells. . Or we may find, in addition to this, 
an increase in cells, which characterizes acute inflammation or hy- 
perplasia of the spleen (see below). 

Infarctions of the Spleen. — Embolic infarctions of the spleen 
are of frequent occurrence. They may be single or multiple, small 
or very large, sometimes occupying half of the organ. They are in 
general approximately wedge-shaped, corresponding to the area of 
tissue supplied by the occluded artery. They may be heemorrhagic, 
i.e., red, or they may be white (see page 62). Infarctions, originally 
red, may become white after a time from changes in the blood pig- 
ment. They may usually be seen as dark-red, reddish-white, or 
white, hard, sometimes slightly projecting areas on the surface of the 
organ. Not infrequently the centre of the infarction is light in color, 
while the peripheral zone is dark-red. A layer of fresh fibrin is 
sometimes seen over the surface of the infarction. The general as 
well as the microscopical appearances which they present depend 
largely upon the age of the infarction. In the earlier stages the 
haemorrhagic infarctions present little more under the microscope 
than a compact mass of red blood cells, among which may be seen 
the compressed necrotic parenchyma. The white infarction may 
show at first in a general way the usual splenic structure, but the 
entire tissue is in a condition of coagulation necrosis. The tissue 
may disintegrate and soften, and be more or less completely ab- 
sorbed, with or without fatty degeneration. A zone of inflamma- 
tory tissue may appear around the infarction and upon the capsule, 
and this tissue, becoming denser, assumes the characters of cicatri- 
cial tissue and contracts around the unabsorbed remnant of the in- 
farction, so that finally nothing may be left but a dense mass of 



624 THE SPLEEN. 

fibrous tissue, which frequently draws in the surface, causing more 
or less distortion of the organ. This cicatrix may be pigmented or 
white. 

If the embolus be of an infectious, irritating nature, in addition 
to its mechanical effects there may be suppuration, gangrene, and 
the formation of abscess. There may be perforation of the capsule 
and fatal peritonitis. 

INFLAMMATION. 

Acute Hyperplastic Splenitis (Acute Splenic Tumor). — The 
conditions under which acute inflammation of the spleen occurs 
have already been mentioned under active hyperaemia, with which 
it is usually associated. It is a frequent though not a constant ac- 
companiment of the acute infectious diseases, and seems in all cases 
to be a secondary lesion. The spleen is enlarged, sometimes to two 
or three times its normal size. On section the pulp is soft, often 
almost diffluent, and projects upon the cut surface. The color is 
sometimes dark-red, sometimes grayish-red, or mottled red and gray. 
The trabeculse and glomeruli are usually concealed by the swollen 
and softened pulp, but the glomeruli are sometimes unusually promi- 
nent. 

Microscopical examination shows the marked increase in size to 
be due in part to the hyperemia; in part to a swelling and increase 
in the number of cells, sometimes of the pulp, sometimes of the 
glomeruli, or of both. We find large, multinucleated cells ; cells 
resembling the ovoidal and polyhedral cells of the pulp, but larger 
and with evident division of the nuclei. Cells resembling leuco- 
cytes may be present in large numbers, and larger and smaller cells 
in a condition of fatty degeneration, or containing pigment, are 
often seen. The elongated cells lining the cavernous veins may be 
swollen or increased in number. Not infrequently larger and 
smaller cells are found which contain structures looking like red 
blood cells or their fragments. In some cases, particularly in scar- 
latina, hyperplasia of the glomeruli is a prominent feature. In some 
cases, particularly in typhus and recurrent fevers, the cells of the 
glomeruli undergo marked degenerative changes, so that they may 
form small softened areas looking like little abscesses. Small ne- 
crotic areas, often associated with localized suppuration, are some- 
times found in typhus and typhoid fever, scarlatina, etc. , and may 
be due to infectious emboli. As the primary disease runs its course 
t&e swelling of the spleen subsides, the capsule appears wrinkled, 
the color becomes lighter, and sometimes the organ remains for a 
long time, or permanently, small and soft. 

The cause of these marked changes in the spleen in infectious 
diseases is not understood, It seems probable that they are due to 



THE SPLEEN. 625 

the lodgment in the organ of some deleterious materials which have 
found access to the blood. Whether these materials are bacteria, or 
products of the life processes of bacteria, or something entirely 
apart from these, we do not in many cases know. Bacteria have, 
indeed, in many cases been found in the organ under these condi- 
tions, but by no means with the frequency and abundance which the 
commonness and prominence of the lesion would lead us to expect 
if it were in all cases due to their presence. 

Suppurative Splenitis (Splenic Abscess). — Small abscesses may 
be found in the spleen as the result of minute infectious emboli, and 
these may coalesce to form larger abscesses ; but larger and smaller 
abscesses may form in the spleen without evidence of their embolic 
origin. Sometimes the entire parenchyma is converted into a soft, 
necrotic, purulent mass surrounded by the capusle. It is rare for 
simple infarctions to result in abscess, but it does occasionally occur. 
Abscess of the spleen may occur from the propagation of a suppu- 
rative inflammation to the organ from adjacent parts ; from peri- 
nephritic abscesses, ulcer and carcinoma of the stomach, etc. Ab- 
scesses of the spleen may open into the peritoneal cavity, inducing 
fatal peritonitis, or, owing to an adhesive inflammation, the opening 
may occur into the post-peritoneal tissue, into the pleural cavity, 
lung, stomach, intestines, or it may open on the surface. On the 
other hand, the contents of the abscess may dry, shrink, and be- 
come encapsulated and calcified. Abscesses may occur in ulcera- 
tive endocarditis, pyaemia, typhoid fever, and more rarely in inter- 
mittent fever, and under a variety of other conditions whose nature 
is unknown to us. 

Chronic Indurative Splenitis (Chronic Splenic Tumor). — There 
may be, as we have already seen, a new formation of connective 
tissue in the spleen as a result of chronic congestion or infarctions, 
or about abscesses. But there is a more diffuse formation of con- 
nective tissue, usually in the nature of an hyperplasia, which oc- 
curs under a variety of conditions, and is now marked and exten- 
sive, and again comparatively ill-defined. It is always associated 
with more or less extensive changes in the parenchyma. In its 
most marked form it is found in chronic malarial poisoning, and 
under these conditions it may be found not only in persons who have 
suffered from repeated attacks of intermittent fever, but also in those 
who have not thus suffered but have resided in malarial regions. 
The enlarged spleen is often called "ague cake." Similar condi- 
tions, though usually less marked, may occur in congenital and ac- 
quired syphilis, from prolonged typhoid fever, and as a result of 
acute hyperplastic splenitis from various causes, and also in leukaemia 
and pseudo-leukaemia. 
50 



626 



THE SPLEEN. 



The gross appearance of the spleen in chronic indurative splenitis 
varies greatly, both in the size of the organ and in the appearance of 
the section. The spleen may be enormously enlarged or it may be 
of about normal size. It is usually, however, enlarged. The cap- 




Fio. 303.— Chronic Indurative Splenitis. 
Showing swelling or proliferation of the lining cells of the cavernous veins. 

sule is usually more or less thickened, frequently unevenly so. The 
consistence is usually considerably increased, but this is not always 
the case. The color and appearance of the cut surface present 




Fig. 304.— Chronic Interstitial Splenitis. 
a, thickened capsule; 6, thickened trabecule; c, dilated cavernous veins; d, dense pulp tissue 
with obliterated cavernous veins. 



much variation. It may be nearly normal or it may be grayish, or 
dark-brown, or nearly black. The color may be uniform or the sur- 
face may be mottled. The glomeruli may be scarcely visible or 



THE SPLEEN. 



627 



-very prominent ; the trabecule are in some cases nearly concealed by 
the pulp ; in others they are large, prominent, and abundant, so that 
the surface is crossed in all directions by an interlacing network of 
broader and narrower irregular bands, between which the red or 
brown or blackish pulp lies. 

Not less varied are the microscopical appearances of the spleen 
under these conditions. In one class of cases there is more or less 
uniform hyperplasia of both pulp and interstitial tissue. The paren- 
chyma cells are increased in size and number ; there may be swell- 
ing and proliferation of the lining cells of the cavernous veins (see 
Fig. 303). The reticulum of the pulp, as well as that of the glome- 
ruli, and also the trabeculse, are thickened. In another class of 
cases the thickening of the reticular and trabecular tissue, either uni- 
formly or in patches, is the prominent feature (Fig. 304), while the 
changes in the pulp are rather secondary and atrophic. In both 
forms irregular pigmentation is frequent, the pigment particles being 




Fig. 305.— Malarial Spleen. 
Showing thickening of the trabecular network of the pulp, with pigmentation of the pulp cells. 



deposited either in the cells of the pulp or glomeruli, or in the new- 
formed interstitial tissue (Fig. 305). Finally, there are all interme- 
diate forms of induration between those described, and the changes 
are by no means uniform in the same organ. When these spleens 
are large they are liable to displacement. 

Syphilitic Splenitis. — This lesion may present itself as an in- 
durative process due to the formation of new connective tissue, and 
present no distinct morphological characteristics. In rare cases, 
however, gummata may be present in connection with the new 
fibrous tissue ; then the nature of the lesion becomes evident. 

Tuberculous Splenitis. — This lesion is secondary, either to tuber- 
cular inflammation in some other part of the body, or is the result of 
f he general infection in acute general miliary tuberculosis. The tuber- 
cles may be very numerous and still invisible to the naked eye, or they 
may be just visible, or as large as a pin's head or thereabouts, and 
Very thickly strewn through the organ or sparsely scattered. In other 



(328 THE SPLEEN. 

cases the tubercles are larger, sometimes as large as a pea, and they 
are then usually not very numerous. Microscopically they present the 
usual variety of structure, sometimes as simple tubercle granula, 
sometimes as conglomerate tubercles ; they may consist simply of a 
collection of small spheroidal cells, or there may be larger polyhedral 
cells and giant cells with a well-defined reticulum. Cheesy degene- 
ration occurs under the usual conditions. Tubercle bacilli are usu- 
ally present, particularly in the more acute forms, sometimes in 
small, sometimes in enormous numbers. They seem to be especially 
abundant in acute general miliary tuberculosis of children. These 
tubercles may be formed in the glomeruli, in the walls of the smaller 
arteries, in the pulp tissue, and in the trabeculse and capsule. Owing 
to the peculiar character of the spleen tissue the earlier stages are 
not readily recognized, since simple collections of small spheroidal 
cells are not distinctly outlined against the normal tissue. There is 
frequently a moderate swelling of the spleen, owing to hypersemia 
and hyperplasia of the parenchyma. 

Perisplenitis. — Acute inflammation of the capsule of the spleen 
may occur as a part of a general or localized peritonitis, or as a re- 
sult of lesions of the spleen itself, such as infarctions, abscesses, and 
acute hyperplastic inflammation. Under these conditions a fibrinous 
pellicle, with more or less pus, may be formed on the surface of the 
organ. Chronic perisplenitis, resulting in the production of new 
connective tissue, either in patches or as a more or less general thick- 
ening of the capsule, is of frequent occurrence. It may follow acute 
inflammation of the capsule, or be a part of general or localized 
chronic peritonitis. It is common in connection with chronic indura- 
tive splenitis, and it may occur from unknown causes. Sometimes 
the capsule is three or four mm. in thickness over a considerable 
area ; sometimes very small nodular thickenings or papillary projec- 
tions occur. As a result of this process adhesions, sometimes very 
extensive, may form between the spleen and adjacent parts. The 
thickened capsule is sometimes more or less extensively calcified. 

Alterations of the Spleen in Leukcemia and Pseudo-Leukoemia. 
— The lesions of the spleen are essentially the same under both of 
these conditions. They consist, in general, of an hyperplasia, some- 
times most marked in one, sometimes in another of the structural 
elements of the organ, but usually they all participate in the altera- 
tions. The changes which occur in the earlier stages are but little 
known. The gross appearances of the spleen, as we find them in 
persons dying of either of the above diseases, present considerable 
variation. They are usually enlarged and sometimes are ten or 
fifteen times the normal size. They are usually hard, but are some- 
times of the ordinary consistence, or softer. The capsule is usually 



THE SPLEEN. 629 

thickened and rough. The section of the spleen may be of a uniform 
dark -red color, but it is more frequently mottled red and gray. 
Sometimes the glomeruli are inconspicuous, but they are very often 
enlarged and prominent. They may be two to four mm. in diameter, 
and, owing to an infiltration of the arterial sheaths with lymph cells, 
may appear to the naked eye as grayish, round or elongated bodies, 
arranged along branching, interrupted, grayish streaks. The trabe- 
cula may be greatly thickened, as also the reticulum of the pulp, so 
as to be evident to the naked eye. Brown or black pigment may be 
collected around the glomeruli or in the pulp. Hemorrhagic infarc- 
tions or circumscribed extravasations of blood may further compli- 
cate the picture. 

Microscopically the appearances are essentially the same as those 
above described in acute hyperplasia and in chronic interstitial sple- 
nitis, depending upon the stage and variety of the disease. Owing 
to the great size which some of these spleens attain they are liable to 
displacement, and they may interfere by pressure with the functions 
of neighboring organs. 

DEGENERATIVE CHANGES IN THE SPLEEN. 

Atrophy. — The spleen may become atrophied in old age ; as a 
result of prolonged cachexise, and in connection with profound and 
persistent ansemia ; or, more rarely, from unknown causes. The 
capsule may be wrinkled and thickened, the color pale, the trabecula 
prominent, the consistence increased. The change is largely in the 
pulp, whose parenchyma cells are decreased in number. . 

Amyloid Degeneration. — This degeneration may affect the glo- 
meruli or the pulp tissue, or both together. When confined to the 
glomeruli the spleen may or may not be enlarged, and the cut sur- 
face is more or less abundantly sprinkled with round or elongated, 
translucent bodies resembling considerably in general appearance 
the grains of boiled sago. These are the waxy glomeruli. Such 
spleens are often called "sago spleens" (Fig. 306). Microscopical 
examination shows that the degeneration is confined to the walls of 
the arteries, capillaries, and reticulum of the glomeruli, with atrophy 
and disappearance of the lymphoid cells. 

In other cases, either with or without involvement of the glo- 
meruli, there is waxy degeneration of the blood vessels and reticu- 
lum of the pulp, which may occur in patches or be general and 
more or less excessive. If the alteration is general and consider- 
able the spleen is enlarged, its edges rounded, its consistence in- 
creased. On section it appears translucent, and the distribution of 
the degenerated areas may be readily seen by holding a thin slice 
up to the light. The spleen may be alone affected, or there may be 



6d0 THE SPLEEN. 

similar degenerations in other organs. The general conditions under 
which this lesion occurs, and the methods of staining and studying,, 
are given on page 100. 

Pigmentation of the spleen may occur as the result of the de- 
composition of haemoglobin in the organ under a great variety of 
conditions : thus after haemorrhagic infarctions, small multiple haem- 
orrhages, acute hyperplastic splenitis, etc. Or the pigment may 
be anthracotic and be brought to the organs from the lungs or 
bronchial glands (see page 106). Bile pigment may also be deposited 
in the spleen in jaundice. The pigment may lie in the walls of the 
smaller arteries, in the cells and reticulum of the pulp, or free in the 
latter tissue, or in the follicles. It is usually quite unevenly dis- 



Fig. 306.— Amyloid Degeneration op Glomeruli of the Spleen— " Sago Spleen/ 1 
The " waxy " portions are stained pink. 

tributed. The pigment may be red, brown, or black. According 
to Weigert anthracotic pigment may be sometimes seen with the 
naked eye in the periphery of the glomeruli as dark crescents. 

Primary tumors of the spleen are rare. Small fibromata, sar- 
comata, and cavernous angiomata sometimes occur. Sarcomata 
and carcinomata may occur in the spleen secondarily either as me- 
tastatic tumors or by extension from some adjacent part, as the sto- 
mach. Dermoid cysts are described, but are rare. Other larger 
and smaller cysts, whose mode of origin is in most cases obscure, 
not infrequently occur. 

PARASITES. 

Pentastomum denticulatum is not infrequently found in the- 
spleen, usually encapsulated and calcified. Cysticercus is rare. 



THE SPLEEN. 6dl 

Ecliinococcus is occasionally found, and, if the cysts are large or 
numerous, may cause more or less extensive atrophy of the organ. 

Various forms of bacteria have been found in the spleen. Micro- 
cocci have been found in pysemia, small-pox, ulcerative endocar- 
ditis, diphtheria, and under other conditions. The Bacillus anthra- 
cis occurs here in anthrax ; the Bacillus tuberculosis in tubercular 
inflammation ; and bacilli have been described in typhoid fever. 
Spirochete Obermeieri may be found in relapsing fever. 

MALFORMATIONS AND DISPLACEMENTS. 

The spleen may be absent in acephalous monsters, and with de- 
fective development of other abdominal viscera. Very rarely it is 
absent in persons who are otherwise perfectly developed. Small 
accessory spleens, from the size of a hazelnut to that of a walnut, 
are not infrequent. They usually lie close to the spleen, but may 
be considerably removed from it ; thus they have been found em- 
bedded in the head of the pancreas. Two spleens of about equal 
size have been observed. The form of the spleen is subject to con- 
siderable variation. It may be made up of several distinct lobes. 
It may be displaced congenitally or as the result of disease. It may 
be on the right side in transposition of the viscera. As the result 
of congenital defects in the diaphragm the spleen may be found in 
the thorax ; or in deficient closure of the abdominal wall it may, 
together with other abdominal viscera, be found outside of the body. 

The spleen may be pressed downward by any increase in the con- 
tents of the thorax. It may be fastened by adhesions to the concave 
surface of the diaphragm, so that its long axis is nearly horizontal 
instead of vertical. It may be displaced by changes in the contents 
of the abdominal cavity. If the organ is increased in size it fre- 
quently becomes tilted, so that its lower border reaches the right 
iliac region. If the ligaments are too long congenitally, or if they 
are lengthened by traction, and if the organ is at the same time in- 
creased in weight, it may become very movable. It may sink down- 
ward, with its hilus turned upward ; or it may be rotated on its axis, 
and, owing to torsion of the vessels thus produced, the organ may 
atrophy ; or the pressure of the ligaments and vessels across the 
duodenum may cause occlusion of the gut. 



THE PANCREAS. 



The diseases of the pancreas appear, so far as we know, with a 
few exceptions, to be of little practical importance ; that is, they do 
not often give rise to symptoms of disease or cause death, but the 
lesions are found in the bodies of persons dead from other diseases. 
It is probable, however, that in many cases their apparent insignifi- 
cance is due to our lack of knowledge of the interference with func- 
tions which lesions of the gland induce, and to the incomplete exami- 
nation of the pancreas which is so common at autopsies. 

Hemorrhage into the substance of the pancreas may occur as the 
result of injury 1 ; in the hemorrhagic diathesis ; in connection with 
valvular diseases of the heart or interference with the portal circula- 
tion ; or in connection with extensive fatty degeneration and fat 
necrosis of the organ. Such haemorrhages may be minute or exten- 
sive. Several cases of sudden death are recorded in which the only 
discoverable lesion was an extensive haemorrhage into the substance 
of the gland*' and the tissue about it. In these cases it has been as- 
sumed that death was caused by interference with the heart's action, 
through pressure on the solar plexus and semilunar ganglion, but it 
may be due to other causes (see below, Fat Necrosis). The haemor- 
rhage may be moderate and limited to the pancreas, or it may ex- 
tend into the subperitoneal tissue for a considerable distance. 

Haemorrhage of the pancreas may be associated with acute in- 
flammatory changes and with more or less extensive gangrene of 
the organ. The gangrenous pancreas may be more or less encapsu- 
lated ; it may lie, bathed in pus, in the abdominal cavity ; it may. 
by ulceration of the intestinal wall, get into the gut and be dis- 
charged with other intestinal contents. 

INFLAMMATION. 

In some cases of typhoid fever, pyaemia, yellow fever, and other 
acute infectious diseases, the pancreas is red, swollen, and cedema- 
tous. Microscopically the most prominent lesion is a swelling and 

1 Consult Lieth, "Rupture of Pancreas, " Lancet, September 28th, 1895. 



THE PANCREAS. 633 

undue granulation of the glandular epithelium, and hypersemia. 
This condition is known as Parenchymatous Pancreatitis. 

Suppurative Pancreatitis is not very common, and may be 
primary or due to the extension of a suppurative inflammation from 
adjacent or distant parts of the body. There may be a diffuse infil- 
tration of the organ, with pus cells or larger and smaller abscesses. 
The abscesses may open into the gastro-intestinal canal or into the 
peritoneal cavity. The causes of primary suppurative pancreatitis 
are often most obscure. . It may be associated with fat necrosis and 
with haemorrhage and gangrene of the pancreas. 

Chronic Interstitial Pancreatitis (Cirrhosis of the Pancreas). — 
This lesion consists in an increase of interstitial connective tissue, 
which may be general or confined to some particular portion of the 
gland. The organ is sometimes enlarged, sometimes smaller than 
normal. It is usually dense and hard ; secondary atrophy of the 
parenchyma regularly occurs. It may be due to chronic inflamma- 
tory processes in the vicinity of the organ. 

Syphilitic Inflammation. — Chronic interstitial pancreatitis is 
frequently found in congenital syphilis of the new-born, and the gross 
and microscopical lesions are similar to those above described. It is 
not definitely established whether or not a similar lesion may be 
caused by acquired syphilis. Gummata are very rare in the pan- 
creas, but have been described in congenital syphilis in very young 
children. 

Tuberculous Inflammation. — Larger and smaller tubercles and 
tubercular, cheesy nodules are occasionally found in the pancreas in 
connection with acute general miliary tuberculosis or with tubercular 
inflammation in some other organ, particularly with that of adjacent 
lymph nodes, the lungs, and the intestine. 

DEGENERATIVE CHANGES IN THE PANCREAS. 

Atrophy of the pancreas may occur in old age and as a result of 
pressure from tumors or other adjacent structures. Marked atrophy 
of the pancreas is found in a certain proportion of cases of diabetes 
mellitus, but it is not constant. 

Fatty Degeneration of the parenchyma cells may occur, and in 
some cases is so extensive as to lead to nearly complete destruction 
of their protoplasm. 

Fatty Infiltration, which should be distinguished from fatty 
degeneration, consists in the accumulation of fat in the interstitial 
tissue of the gland. This may be so excessive as to cause nearly 
entire destruction of the gland structures. Under these conditions 
the outline of the organ may be preserved, the fat being enclosed by 
the capsule. 



634 



THE PANCREAS. 



Amyloid Degeneration. — This usually occurs in connection with 
similar degeneration in other organs, and is confined to the walls of 
the blood vessels and the interstitial tissue. 

Fat Necrosis. — A very peculiar lesion of the fat tissue, most 
frequently seen in the fat tissue about the pancreas or between its 
lobules, but sometimes in fat tissue in other parts of the body, has 
been a few times described and called fat necrosis. White or yel- 
lowish nodules, varying from the size of a pin's head to that of a pea 
or larger, are seen embedded in the fat, the central portion being 
often soft and grumous and readily squeezed out. They are some- 
times calcined and sometimes surrounded by a connective-tissue 







v~ ~ J « .T) - >, 



. ... 



M% 









?>/, 




Fig. 307.— Fat Necrosis in the Pancreas. 
Drawn from a specimen prepared by Dr. fra Van Gieson and reported to the New York Patho- 
logical Society, 1888. 

capsule. Microscopical examination shows degeneration and dis- 
integration of the fat tissue (Fig. 307). They are most frequently 
found in marasmatic persons. When the lesion is extensive, accord- 
ing to Balser, it may cause death, either directly or by inducing 
haemorrhage. Some of the extensive haemorrhages about the pan- 
creas, above mentioned, may be caused in this way. 1 

1 For a detailed consideration of acute inflammation, haemorrhage, gangrene, and fat 
necrosis of the pancreas, with bibliography, consult Fitz, Middleton Goldsmith lecture 
for 1889 on "Acute Pancreatitis," Transactions New York Pathological Society, 
1889. For special studies on fat necrosis consult Langerhans, Virchow's Archiv, 
Bd. cxxii., p. 252, and in the " Festschrift " for Virchow's seventy-first birthday. 



THE PANCREAS. 635 

TUMORS. 

Carcinomata are the most common and important of the tumors 
of the pancreas. They may be primary or secondary. Primary 
carcinomata are most frequently found in the head of the organ, but 
may occur in other parts. The hard or scirrhous form is most com- 
mon, but occasionally soft and succulent and colloid forms are 
found. They are liable to involve adjacent parts by continuous 
growth, and may form metastases in the liver, adjacent lymph 
nodes, etc. Secondary carcinoma in the pancreas may occur in 
carcinoma of the stomach, duodenum, and the gall ducts and gall 
bladder. As a result of carcinoma of the pancreas, aside from the 
extension of the growth, there may be pressure on the ductus chole- 
dochus, with jaundice ; or on the pancreatic duct, with cystic dila- 
tation ; or pressure on the duodenum, with stenosis of the gut ; or 
pressure on the vena cava, or portal vein, or superior mesenteric 
vein, etc. , with disturbances of the circulation. 

Concretions of carbonate and phosphate of lime are frequently 
found in the pancreatic ducts. They are usually multiple, small, 
whitish, smooth, or of rough and irregular shape. Sometimes, how- 
ever, they reach a diameter of more than an inch. They consist 
chiefly of calcium phosphate and carbonate. Besides these free con- 
cretions the walls of the ducts are sometimes encrusted with salts of 
lime. Such concretions may produce dilatation of the pancreatic 
ducts and large cysts, or more rarely abscesses. 

Foreign Bodies. — Gall stones sometimes find their way into the 
pancreatic duct. Ascarides have been found in the ducts in a con- 
siderable number of cases. 

Cysts. — These are mostly due to dilatation of the pancreatic 
ducts. 

1. The entire duct may undergo a uniform cylindrioal dilatation. 
With this cylindrical dilatation we sometimes find associated small 
sacculi. 

2. There may be sacculated dilatations at some points in the 
ducts. These dilatations form cysts of large size, as large even as 
a child's head. Their walls frequently undergo degeneration and 
calcification. These cysts often become filled with blood, and may 
then be mistaken for aneurisms. 

3. The small branches of the pancreatic duct may be dilated so as 
to form a number of small cysts. These cysts are filled with serum, 
mucus, pus, or a thick, cheesy material. 

Cysts of the pancreas may result from old areas of necrosis or 
haemorrhage, and in other ways. 1 

1 Consult Tilger, "Cysts of Pancreas, " Vircb. Arch., Bd. cxxxvii., 348 (bibliog- 
raphy) . 



636 



THE PANCREAS. 



MALFORMATIONS AND DISPLACEMENTS. 

The pancreas may be entirely absent in anencephalous and double 
monsters, and in congenital umbilical hernise. The pancreatic duct 
may be double ; it may open into the duodenum at some distance 
from the biliary duct, or into the stomach. The head of the pancreas 
may be unduly developed, and sometimes even completely separated 
from the rest of the organ, opening into the duodenum with a duct 
of its own. Occasionally there is a small accessory pancreas situated 
beneath the serosa of the duodenum or stomach. 

The pancreas is so firmly bound down that its position is not often 
changed. Sometimes, however, it is found pressed downward by 
tight lacing, displaced by aneurisms, or contained in umbilical and 
diaphragmatic herniee. 






THE SALIVARY GLANDS. 



THE PAROTID, SUBMAXILLARY, AND SUBLINGUAL. 
INFLAMMATION, 

This condition is most frequent and important in the parotid. 
The lesions of the epidemic disease known as mumps are most fre- 
quently confined to the parotid gland of one side, but the submaxil- 
lary and sublingual may be at the same time involved. The gland 
is swollen and there is often oedema of the mucous membrane of 
the mouth and pharynx. Very little is known of the actual minute 
changes which the gland undergoes in this disease. 

Acute parotiditis occasionally occurs as a secondary lesion in a 
variety of diseases, as in typhoid and scarlet fever, pyemia, pneu- 
monia, etc., and by propagation of inflammation from the mouth. 
Under these conditions the inflammation is usually suppurative and 
frequently results in abscess or sloughing. The interstitial tissue 
of the gland is more or less densely infiltrated with pus cells, and 
the parenchyma cells may undergo fatty degeneration and disin- 
tegration. The inflammation may be confined to the gland or it 
may spread to adjacent parts, sometimes causing much destruction 
of tissue, and may give rise to inflammation of the brain or of the 
inner ear, or even to metastatic pysemic abscesses in different parts 
of the body. Healing may occur, with the formation of salivary 
fistulas. 

The submaxillary gland may be involved with the parotid in the 
suppurative inflammation. 

Acute suppurative inflammation of the connective tissue about 
the submaxillary gland is sometimes of serious import. Sloughing 
and gangrene may occur and are apt to spread to adjacent parts. 
Septicaemia, oedema of the glottis, or pneumonia may complicate the 
process and cause death. 

The sublingual gland is not often the seat of inflammation. 

Chronic inflammation, leading to the formation of dense inter- 



638 THE SALIVARY GLANDS. 

stitial tissue, sometimes occurs in the salivary glands. This may 
occur by itself or follow an acute inflammation. 

The Excretory Ducts of the salivary glands may become inflamed 
from the presence of foreign bodies or of concretions formed in them. 
They may become occluded from the presence of calculi or as the 
result of inflammation, and may thus become widely dilated both in 
the main branches and in the finer ramifications. The dilatation of 
Wharton's duct to form larger and smaller cysts containing salivary 
fluid, sometimes gives rise to very large and troublesome tumors 
which constitute one of the forms of ranula. 



TUMORS. 

Fibromata are of occasional occurrence in the parotid. Chon- 
dromata, endotheliomata, sarcomata and fibro- sarcomata, and 
myxomata, or more frequently mixed tumors formed of varied com- 
binations of these, are of frequent occurrence in the parotid and of 
occasional occurrence in the submaxillary gland. These complex or 
mixed tumors are of more frequent occurrence in these glands than 
in any other part of the body, except possibly the ovary. They are 
sometimes rendered still more complicated in structure by the forma- 
tion of cysts, and what has been regarded usually as an atypical 
glandular growth, lending them an adenomatous character. The 
more recent studies upon the mixed tumors of the salivary glands, 
however, have led to the belief that a large part of these complex 
growths are endotheliomata, which are especially prone in these 
regions to undergo secondary degenerative or metaplastic changes. 1 
Carcinomata of the salivary glands are rare. 

Fibrosarcoma and melano-sarcoma have been described. Pri- 
mary carcinoma of these glands is very rare. 

A case of rhabdomyoma of the parotid gland, with evidences of 
atypical development of portions of the gland, has been described by 
one of us. 2 

PARASITES. 

Echinococcus has been observed in the parotid gland. 

1 Volkmann, Deutsche Zeits. f. Chir., Bd. xli., p. 61. 

2 Prudden, "Rhabdomyoma of the Parotid Gland," American Journal of the 
Medical Sciences, April, 1883. 



THE THYROID GLAXD. 1 



Hypercemia of the thyroid gland, often accompanied by consider- 
able enlargement of the organ, may be the result of valvular disease 
of the heart; it occurs in Basedow's disease; it may be temporary or 
permanent, and in the latter case may give rise to the formation of 
new connective tissue. Haemorrhages may occur, causing pigmen- 
tation of the organ. 

Inflammation of the thyroid gland is not very common and may 
occur from a variety of causes. It may result in the formation of 
larger and smaller abscesses or in the production of new connective 
tissue. Tuberculous inflammation, with the formation of miliary 
tubercles, is of infrequent occurrence. Syphilitic inflammation, 
with the formation of gummata, has been described, but is rare. 

Degeneration. — Colloid degeneration of the epithelial cells of 
the gland, and the filling of the alveoli with colloid material, is of 
common occurrence, and when occurring in moderate degree may be 
regarded as a normal event, since a certain amount of this change is 
found in many otherwise apparently normal glands. It may occur, 
however, to such an extent as to constitute a lesion (see below). 

Amyloid degeneration, particularly of the blood vessels, is of in- 
frequent occurrence. 

Hyaline degeneration of the stroma of the thyroid may occur. 

Inflammation (Thyroiditis). — Suppurative inflammation of the 
thyroid is of occasional occurrence. Chronic interstitial inflamma- 
tion, and tuberculous and syphilitic inflammation are rare. 

TUMORS. 

Among the most important of the lesions of the thyroid is the en- 
largement of the organ commonly known as the goitre or struma. 
The enlargement of the gland may occur in several different ways, 
and in only a part of the cases is to be considered as a tumor. Thus, 
a simple hyperemia may, as above stated, cause considerable en- 
largement of the organ, and this is sometimes called struma hyper- 

1 For a study of the normal and pathologic histology of the thyroid, with bibli- 
ography, consult 'Muller, Ziegler's Beitr. z. path. Anat., etc., Bd. xix., p. 127, 1896. 



640 



THE THYROID GLAND. 



cemica. The true goitre, however, consists in the enlargement of 
the old and the formation of new gland alveoli, while with these 
changes there is very frequently associated a greater or less amount 
of colloid degeneration. When there is new formation of gland tissue 
the growth has the character of an adenoma. The hyperplasia may 
occur diffusely, so that the whole gland is more or less enlarged ; or 
it may occur in the form of circumscribed nodules. When the col- 
loid degeneration is prominent, so that the tumor has a gelatinous 
look, it is called colloid struma (Fig. 308). ' Accumulations of 
fluid, blood, colloid, etc., in the old or new-formed alveoli, may cause 
dilatation and atrophy of the walls of the alveoli, so that cysts, some- 




~' ^vuisievx ^ "' 



Fig. 308,— Colloid Struma— Goitre. 
The colloid material filling the alveoli is stained red. 

times of large size, are formed. Thus occurs the cystic struma. 
Again, the blood vessels may undergo marked dilatation, so that we 
may have a telangiectatic struma; or cavernous angiomata may 
form within them. Very frequently all these varieties of lesions are 
present in the same goitre. The appearances maybe rendered still 
more complex by the occurrence of haemorrhages and pigmentation, 
calcification, purulent or indurative inflammation (strumitis), and 
by the not very infrequent association with carcinoma and sarcoma. 
The cause of goitre is not well understood. The growth is, as a rule, 



1 For a consideration of the nature of colloid and its formation in struma see 
Reinbach, Ziegler's Beitr. z. path. Anat. , etc., Bd. xvi., p. 596 (bibliography). 



THE THYROID GLAND. 641 

slow, but occasionally a very rapid enlargement occurs as the result 
of a sudden increase of the colloid degeneration. In many cases even 
very large goitres give rise to but moderate inconvenience, but they 
may assume great significance by encroaching upon neighboring parts. 
Thus death may be caused by pressure on the trachea, oesophagus, 
or on the large vessels. 

Sarcoma, either spheroidal or spindle-celled, may occur as primary 
tumors in the thyroid, either in otherwise normal glands or in con- 
nection with struma. Melano-sarcoma has been observed. Second- 
ary sarcomata are rare. 

Primary carcinoma, both glandular and scirrhous, occurs in the 
thyroid, and, particularly in the softer forms, may spread to adja- 
cent parts and occasionally form distant metastases. 

PARASITES. 

Ecliinococcus cysts have been found in the thyroid. 

MALFORMATIONS. 

The thyroid gland is sometimes very small, either as the result of 
atrophy or as a congenital deficiency. This is most marked in the 
condition called myxcedema (see below). 

It may be irregularly lobulated. There may be small accessory 
glands situated at some distance from the normal position, as in the 
mediastinum or pleura. 

MYXGEDEMA. 

This disease occurs most frequently in middle-aged women, and 
its cause is unknown. The skin of the face is apt to be swollen and 
waxy, causing a peculiar and rather characteristic appearance of the 
features. The skin of the body is apt to be dry and rough, and the 
hair may fall out. Perspiration is, as a rule, diminished. The men- 
tal condition is dull, and loss of memory and insanity may occur. 
Bodily movement and speech are apt to be impaired. 

The fat tissues may be atrophic, and the subcutaneous tissue has 
been shown in some, though not all, of the cases to contain an un- 
usual amount of mucin. In some cases the fibres of the upper layers 
of the corium are crowded apart by fluid. 

The most marked and constant lesion in this disease is an atrophic 
condition of the thyroid gland. The parenchyma of the gland is 
more or less completely replaced by fibrillar connective tissue and by 
new-formed reticular tissue resembling the lymphatic tissue of the 
lymph nodes. 

The general appearance of the atrophied thyroid gland is shown 
in Fig. 309. • 

In a case reported by Hun, which one of us has examined, the 
51 



642 



THE THYROID GLAND. 



lobes of the thyroid measured less than one-half of an inch in dia- 
meter, and the entire gland weighed only about 7.2 gm. (112 grains). 

In addition to the lesion of the thyroid there are apt to be chronic 
endarteritis and chronic diffuse nephritis. In some cases there is an 
accumulation of small spheroidal cells about the smaller blood vessels 
in various parts of the body, and also petechial haemorrhages. 

While the atrophy of the thyroid is the most marked and frequent 
lesion in this disease, our lack of knowledge about the function of 
this gland prevents a definite conception as to the relationship of this 
change to the symptoms. 

By the destruction of the thyroid from disease, or as the result of 
its removal in men and animals, a condition considerably resembling 
myxcedema is apt to be induced. 




Fig. 



-Section of the Atrophied Thyroid Gland in Myxcedema. 



a, interstitial tissue; 6, atrophied lobules with small spheroidal-celled or lymphatic tissue in 
their peripheries. 

Myxcedema appears to be identical with that condition which has 
been described as cachexia strumipriva. 1 

The relationship of an atrophied thyroid to sporadic cretinism is 
worthy of investigation. 2 



1 For detailed descriptions of myxcedema, and the literature, see Hun and Prud- 
den, " Myxcedema, " Am. Jour. Med. Sciences, July and August, 1888, and "Report 
on Myxcedema" in Supplements to the Clinical Society Transactions, vol. xxi., 
London, 1888. 

2 Consult Osier, "Sporadic Cretinism in America, " Trans. Assn. Am. Phys., vol. 
v. , p. 380, 1893, and Ncyes, N. Y. Med. Jour. , March 14th, 1896. 



THE THYROID GLAXD. 643 

EXOPHTHALMIC GOITRE. 

(Basedow's Disease, Graves' Disease.) 

The characteristic lesions of this disease are unilateral or bilateral 
enlargement — largely hypersemic — of the thyroid and protrusion of 
the eyeballs. These lesions are apt to be associated with functional 
disturbance of the heart. 1 

THE THYMUS. 

Small accessory thymus glands are occasionally found near the 
thyroid. 

The thymus occasionally but not usually persists until youth or 
middle age instead of undergoing the usual developmental atrophy. 

Small haemorrhages are described in the thymus of young chil- 
dren as the result of venous congestion in asphyxia, etc. They may 
also occur in the hemorrhagic diathesis. 

Suppurative inflammation of the thymus is of occasional occur- 
rence, and is usually secondary to a similar inflammatory process in 
some other part of the body. 

Tubercular and syphilitic inflammation of the thymus are de- 
scribed. The sarcomata are the most common tumors of the thymus. 2 

1 On the relationship between the thyroid and Basedow's disease consult Eulen- 
berg, Deutsche med. YVochensch., October -1th, 1894; also Edmunds, Jour, of Path- 
ology and Bacteriology, vol. iii., p. 488, 1896; Fame/', Yirchow's Archiv, Bd. 
cxliii., p. 509, 1896 (bibliography) ; Kinnicutt, Med. Record, April 18th. 

- On the relationship of hyperplasia in a persistent thymus to Hodgkin's disease 
consult Brigidi and Piccoli, Ziegler's Beitr. z. path. Anat., etc., Bd. xvi., p. 388. 



THE SUPEAREBTAL BODIES- ADBENALS. 



MALFORMATIONS . 



In acephalic and other monsters the suprarenal capsules may be 
atrophied or entirely absent. Sometimes in well-formed adults these 
organs cannot be discovered. 

There may be little rounded nodules loosely attached to the surface 
of the capsules and having the same structure. 

Accessory and misplaced adrenals are not uncommon. 

If one of the kidneys is absent or in an abnormal position its 
suprarenal capsule usually retains its proper position. 

HEMORRHAGE. 

In children, soon after birth, it is not very infrequent to find large 
haemorrhages in one of the capsules, converting it into a cyst rilled 
with blood. The same lesion has been observed in a few cases in 
adults. 

THROMBOSIS. 

Klebs describes a case of capillary thrombosis of the cortex in 
both capsules in a woman after excision of the knee joint. 



INFLAMMATION. 

Suppurative inflammation, with the formation of abscesses, has 
been seen in a few cases. 

The most frequent lesion of the suprarenal capsules is tuberculous 
inflammation. They are usually increased in size, their surfaces 
are smooth or nodular. The normal structure of the gland is lost, 
and is replaced by tubercle tissue, connective tissue, and cheesy 
matter (see Addison's Disease). 

Syphilitic inflammation, with and without the development of 
gummata, is of occasional occurrence. 

1 For consideration of relationship of adrenals to nervous system see Alexander, 
Ziegler's Beitr. z. path. Anat. , Bd. xi., p. 145 (bibliography). 



THE SUPRARENAL BODIES — ADRENALS. 645 

DEGENERATION. 

Fatty degeneration of the cortical portion of the capsules is the 
rule in the adult. It sometimes occurs in nodular areas. In chil- 
dren under five years of age it is a pathological condition. 

Amyloid degeneration may involve both the cortical and medul- 
lary portions. In the cortex it usually involves only the walls of the 
blood vessels; in the medulla both the blood vessels and the cells of 
the parenchyma may undergo this degeneration. The capsules are 
usually firm and of a grayish, semi-translucent color. 

Pigmentation of the inner cortical zone is frequent in old persons. 

TUMORS. 

Carcinoma of the adrenals is not common. It may be primary, 
but is much more frequently secondary. Either one or both of the 
capsules may be the seat of the new growth. 

Sarcoma occurs as a primary and secondary growth. Probably 
many of the older cases described as cancers were really sarcomata. 

Cylindroma. — Klebs describes a growth of this character in one 
of the adrenals, secondary to a tumor of the same kind in the supra- 
orbital region. He gives to such tumors the name of lymphangioma 
cavernosum. The exact character of these growths is still obscure. 
They consist of irregular follicles and cavities, lined with epithelium, 
and containing peculiar hyalin, structureless bodies. 

Cysts are found, both single and multiple. They are usually 
situated in the cortex. 

Neuroma. — Ganglionic neuromata have been described by Weich- 
selbaum and Freeman. 

Glioma has been described as occurring in the medullary region. 

An hyperplasia of the gland tissue {adenoma or struma lipoma- 
tosa suprarenalis) with fatty degeneration in the form of circum- 
scribed nodules, is described by Yirchow and others. 

Some of the so-called adenomata of the kidney are probably ade- 
nomata of displaced accessory adrenals. 1 

Consult Ulrich, Ziegler's Beitr. z. path. Anat., Bd. xviii., p. 589, 1895. 



THE URINARY APPARATUS. 



THE KIDNEYS. 



MALFORMATIONS. 



Entire absence of both kidneys is sometimes associated with great 
malformation of the entire body. Such foetuses are not viable. 

Absence of one kidney is not uncommon, the left kidney being 
more frequently absent than the right. The absence of the kidney 
may be complete, the ureter being also absent ; there may be an ir- 
regular mass of much-atrophied kidney tissue with connective tissue 
and fat, or there may be only a little mass of connective tissue and 
fat representing the kidney, and a ureter running down to the blad- 
der. The single kidney which is present is usually much enlarged. 
It may be in its natural position or displaced downward. 

Since the extirpation of the kidney has been practised by sur- 
geons it has been found that absence of one kidney is more common 
than was formerly believed. 

When both kidneys are present one of them may be much larger 
than the other. 

Sometimes one kidney will have two pelves or two ureters. 

A rather frequent malformation is the so-called horseshoe kidney. 
The lower ends of the kidneys are joined together by a commissure. 
The commissure is usually composed of kidney tissue, but some- 
times of connective tissue. The two kidneys may be normal, except 
for the commissure ; or their shape, the arrangement of the vessels 
and ureters, and the position, may be unnatural. 

The two kidneys may be united throughout so as to look like a 
single misshapen kidney with two or more pelves and irregular blood 
vessels. The united kidnej^s may be both situated on one side of the 
vertebral column or in the pelvis. 



CHANGES IN POSITION. 



The kidneys may be placed in an abnormal situation, in which 
they are either fixed or movable. 



THE URINARY APPARATUS. 64? 

The change in position is either lateral or downward. When 
displaced downward the kidney may be over the sacrum or below 
this in the cavity of the pelvis. The vessels also have an irregular 
origin and distribution. The kidney is firmly attached in its abnor- 
mal position. 

Movable or wandering kidneys are found in adult life as a result 
of tight lacing, of pregnancy, of overexertion, and of unknown 
causes. They are more frequent in females than in males. The 
right kidney is the one more frequently affected. The blood vessels 
become lengthened and the attachments of the kidney longer and 
looser. 

bright's disease. 

This name is used as a convenient term to group together a cer- 
tain number of diseases of the kidney. This group may be subdi- 
vided as follows : 

I. Acute BrigliVs Disease. 

1. Acute Congestion of the Kidney. 

2. Acute Degeneration of the Kidney. 

3. Acute Exudative Nephritis. 

4. Acute Diffuse Nephritis. 

II. Chronic Bright's Disease. 

1. Chronic Congestion of the Kidney. 

2. Chronic Degeneration of the Kidney. 

3. Chronic Diffuse Nephritis tvith Exudation. 

4. Chronic Diffuse Nephritis without Exudation. 

ACUTE CONGESTION OF THE KIDNEYS. 

Acute congestion is caused by the ingestion of certain poisons, by 
extirpation of one of the kidneys, by severe injuries inflicted on any 
part of the body, by surgical operations, especially those on the 
bladder and urethra, and by over-exertion. We are rarely able to 
obtain human kidneys in the state of acute congestion, for the condi- 
tion is not usually a fatal one. In animals, however, the condition 
can be produced experimentally by cantharidin. It is found that the 
kidneys are enlarged, that the veins, capillaries, and Malpighian tufts 
contain an increased quantity of blood, and that the epithelial cells of 
the cortex tubes are flattened. There may be an exudation of serum 
and an escape of red blood cells from the vessels. 



648 



THE URINARY APPARATUS. 



ACUTE DEGENERATION OF THE KIDNEYS. 

(Acute BrighVs Disease; Parenchymatous Nephritis; Parenchy- 
matous Degeneration.) 

The introduction of certain poisons into the body is regularly fol- 
lowed by changes in the cells of the viscera. The poisons which 
exert this effect may be mineral poisons, such as arsenic, mercury,, 
and phosphorus; or the poisons of infectious diseases, such as diph- 
theria, typhoid fever, etc. According to the quantity and virulence 
of the poison received into the body, there are more or less marked 
changes produced in the cells of the viscera. 







Fig. 310.— Acute Degeneration op the Kidney (Acute Parenchymatous Degeneration). 
From a case of yellow fever, a, the swollen and granular epithelium peeling off and disinte- 
grating; 6, hyalin material in the lumen of the tubule. 

Small doses of such poisons, acting only for a moderate length of 
time, produce simple swelling of the cells. The cells are swollen, 
more opaque, more coarsely granular (Fig. 310). They are not dead, 
nor broken down, nor do they contain any new substances ; the change 
in their appearance is due to the swelling of the network which forms 
a part of every cell. Under these circumstances there are either no 
changes at all in the blood-vessels of the viscera, or a slight conges- 
tion, with, perhaps, a little exudation of serum. 

Larger doses of such poisons, or more virulent poisons, or a longer 



THE URINARY APPARATUS. 649 

duration of the action of a poison, are attended by the deposition in 
the cell bodies of granules of albuminous matter and gloubles of fat. 
At the same time there is a change in the nutrition of the cells, and 
they are often broken and disintegrated. Under these conditions 
there may be considerable congestion of the vessels and an exudation 
of serum. 

Very large doses of such poisons cause the death of the cells of 
the viscera, a death which may take the form of coagulation necrosis 
or of disintegration and breaking down of the cell. With these 
changes there will often be an excessive congestion of the vessels and 
a large exudation of serum and the formation of casts. 

As the kidneys are excreting organs it is rather natural to think 
that the substances which cause degeneration of the renal epithelium 
do so because they are excreted by the kidneys. But, as the same 
poisons produce similar degeneration in many other parts of the body, 
it seems more probable that the effect of the poison is produced in the 
same way that it is in the nerves, the muscles, the liver, and the 
spleen. 

The well-known fact that temporary cutting off of the arterial 
blood from the kidnej'S in animals is followed by degeneration or 
death of the renal epithelium, has led to the idea that degeneration 
of the kidneys, especially in cholera, is due to ischsemia. This 
seems possible, but it is a theory not at all applicable to most cases 
of acute degeneration. 

It is a question of much importance whether the same toxin pro- 
duces degeneration or nephritis according to its dose, or whether two 
or more different toxins are necessary. In scarlatina and diphtheria, 
for example, the rule is that acute degeneration comes in the early 
days of the disease, acute exudative nephritis in the late days of the 
disease, and acute productive nephritis just after the close of the 
disease. Does this mean three different toxins, or that the same toxin 
varies at different stages of the disease, or that the only differences 
is in the dose? 

For clinical purposes the recognition of the fact that acute degen- 
eration is the ordinary lesion of the infectious diseases is of much 
practical importance. 

The gross appearance of the kidney varies with the extent of the 
degeneration. In the ordinary mild cases, such as accompany pneu- 
monia, the kidney is a little larger, the cortical portion a little 
thicker and paler. In the severe cases, such as accompany acute 
yellow atrophy of the liver, the kidney is considerably enlarged and 
more or less congested. 



650 



THE URINARY APPARATUS. 
ACUTE EXUDATIVE NEPHRITIS. 



(Acute Bright' s Disease; Parenchymatous Nephritis; Tubal 
Nephritis; Desquamative Nephritis; Catarrhal Nephritis; 
Croupous Nephritis; Glomerulo- Nephritis.) 

Acute exudative nephritis is frequently a primary inflammation, 
occurring either after exposure to cold or without discoverable 
cause. It may complicate any one of the infectious inflammations 





X 



Fig. 311.— Acute Exudative Nephritis. 
Showing cortex tubes containing coagulated ma'ter and with flattened epithelium. 

or diseases, but is especially common with scarlet fever. It is one 
of the forms of nephritis which are apt to accompany pregnancy. 

The infectious diseases are often complicated with inflammations 
of different parts of the body. The probable causes of these are the 
chemical poisons produced by the growth of the pathogenic bacteria 
belonging to each disease. It seems also that the poison of each dis- 
ease has a preference for particular portions of the body. In rheuma- 
tism the joints and heart are regularly inflamed; in measles the 
bronchi; in scarlet fever and diphtheria the throat and the kidneys. 



THE URINARY APPARATUS. 



651 



As regards the presence of bacteria in the kidneys themselves as 
exciting causes of inflammation our knowledge, save for certain 
phases of suppurative lesion, is incomplete. 

Whether nephritis in puerperal women and after exposure to cold 
is due to disturbances of circulation or to some poison in the blood, is 
not certain. 

The nephritis has the ordinary characters of an exudative inflam- 




Fig. 312.— Acute Exudative Nephritis. 
Showing tubes with flattened epithelium and containing red and white blood cells and casts. 



mation : congestion, an exudation of blood plasma, an emigration of 
white blood cells, and a diapedesis of red blood cells; to which may 
be added swelling or necrosis of the renal epithelium and changes in 
the glomeruli. 

In the milder cases we find the inflammatory products— serum, 
casts, white and red blood cells — in the urine. But in the kidneys 
after death we find no lesions, unless it may be a few casts in the 
straight tubes. The morbid process is confined to the blood vessels 



652 



THE URINARY APPARATUS. 



of the kidney, and its only result is the exudation into the renal 
tubules. 

In the more severe cases we find the kidneys large and smooth, 
the cortex thick and white, or white mottled with red, or the entire 
kidney intensely congested. If the stroma is infiltrated with serum 
the kidney is succulent and wet ; if the number of pus cells is very 
great there will be little, whitish foci in the cortex. 

There are, besides the exudation, changes in the tubes, the stroma, 
and the glomeruli. All the changes are most marked in the cortical 
portion of the kidney. 




Fig. 313.— Acute Nephritis, x 850 and reduced. 
Paris green tM-enty hours before death. 



In the tubes the epithelium may be flattened, or swollen, opaque, 
and detached from the walls of the tubes. There may be a uniform, 
symmetrical dilatation of all the cortex tubes. The tubes may be 
empty or they may contain coagulated matters in the form of irregu- 
lar masses and of hyalin cylinders. The irregular masses are found 
principally in the convoluted tubes; they seem to be formed by a 
coagulation of substances contained in the exuded blood plasma, and 
are not to be confounded with the hyalin globules so often found in 
normal convoluted tubes. 



THE URINARY APPARATUS. 



653 



The hyalin cylinders are more numerous in the straight tubes, 
but are also found in the convoluted tubes. They are also formed of 
matter coagulated from the blood plasma, and are identical with the 
casts found in the urine. The tubes may also contain red and white 
blood cells. 

The hyalin casts, the coagulated matter, and the red and white 
blood cells may be all found in the urine while the nephritis is going 
on, 

In some cases there is an excessive emigration of white blood 
cells. This excessive emigration is not necessarily attended with 




Fig. 314.— Acute Nephritis occurring -with. Acute General Tuberculosis, X 850 and reduced. 



exudation of the blood serum, and so the urine of these patients may 
contain no albumin. 

The white blood cells are not found equally diffused throughout 
the kidney, but are collected in foci in the cortex. These foci may 
be very minute or attain a considerable size. They do not resemble 
the suppurating foci seen with embolism or with pyelo-nephritis. 

In the glomeruli we find considerable changes. The cavities of 
the capsules may contain coagulated matter and white and red blood 
cells, just as do the tubules. The capsular epithelium may be 



654 



THE URINARY APPARATUS. 



swollen, sometimes so much so as to resemble the tubular epithelium, 
and this change is most marked in the capsular epithelium near the 
entrance of the tubes. 

The most noticeable change, however, is in the capillary tufts of 
the glomeruli. These capillaries are normally covered on their outer 
surfaces by flat, nucleated cells, so that the tuft is not made up of 
naked capillaries, but each separate capillary throughout its entire 
length is covered over with these cells. There are also flat cells which 




Fig. 315.— Acute Exudative Nephritis. 
Showing a glomerulus with growth of tuft cells and thickening of the capsular epithelium. 



line the inner surfaces of the capillaries, but not continuously as in 
the case with capillaries in other parts of the body. 

In exudative nephritis the swelling and growth of cells on and in 
the capillaries change the appearance of the glomeruli. They are 
larger, more opaque; the outlines of the main divisions of the tufts 
are visible, but those of the individual capillaries are lost. This 
change in the appearance of the glomeruli is due to the swelling and 
growth of the cells on and in the capillaries (Fig. 316). 



THE URINARY APPARATUS. 



655 



In very severe cases the growth of the cells on the tufts is so con- 
siderable that they form large masses of cells between the glomerulus 
and its capsule. 

The walls, of the arteries in the kidneys may be thickened by a 
swelling of their muscular coats. 

Acute exudative nephritis is regularly a transitory lesion. It 
may, indeed, be so severe as to destroy life in a short time. But, as 





m 



W^M&^^W '■■'- J "7^ 




lifil 



Fig. 316.— Acute Nephritis. 



Showing the swelling and growth of cells in and on the capillaries of a glomerulus in a case 
of scarlatina. 

a rule, if the patients do recover from it they recover completely and 
the kidnevs return to their natural condition. 



ACUTE PRODUCTIVE (OR DIFFUSE) NEPHRITIS. 

{Acute BrighVs Disease; Parenchymatous Nephritis; Croupous 
Nephrit is; Glomerulo-X ephritis .) 

This is an acute inflammation of the kidneys, characterized by 
exudation from the blood vessels, a growth of new connective tissue 
in the stroma,' and changes in the epithelium and the glomeruli. 



656 



THE URINARY APPARATUS. 



The kidneys are increased in size, the capsules are not adherent, 
the surfaces are smooth. The cortical portion is red, or white, or 
mottled. The mucous membrane of the pelvis is sometimes con- 
gested. Of the tubules in the cortex, in some the epithelium is 
flattened, in some there is coagulated matter or casts, in some the 
epithelium is swollen, degenerated, or contains globules of fat. In 
those parts of the cortex in which there is a growth of new connec- 
tive tissue, the tubes may be atrophied. The tubules of the pyramids 
show but little change , except that they may contain casts. In the 
stroma of the cortex there is a growth of new connective tissue, 




Fig. 31?. — Acute Productive Nephritis. 
A vertical section of the cortex, showing the wedge-shaped growth of connective tissue. 



varying in different kidneys as to the relative proportion of cells and 
basement substance. This new tissue in many of the kidneys follows 
the line of the arteries which run up into the cortex in the form of 
elongated wedges (Fig. 317). But in other kidneys the new tissue 
is diffuse, or in irregular patches. 

Manjr of the glomeruli show only an increase in the size and 
number of the cells which cover the capillaries, with some swelling 
of the capsule cells. But in others there is an extensive new growth 
of capsule cells which compresses the tuft of vessels. This growth 
of new cells from the capsule cells must not be confounded with ac- 



THE URINARY APPARATUS. 6o7 

cumulations of white blood cells within the capsules, nor with the 
growth of new cells on the walls of the capillaries. The glomeruli 
which are changed in this way are in groups, each group correspond- 
ing to some one artery. 

The whole picture of the nephritis is that of a combination of 
exudative and productive inflammation. 

When such a nephritis becomes chronic it is often possible to fol- 
low its course for many years, and to see at the end of that time that 




^5 * .<-% ■ * £ * - B 

■ 



:./*#^ 



Fig. 318. —Sub-acute Productive Nephritis. 
Glomerulus showing the growth of capsule cells. 



the anatomical changes in the kidneys are of the same kind, but 
much more extensive. 

This is the most serious and important of the forms of acute ne- 
phritis, for the reason that its lesions are from the first of a perma- 
nent character. It does not follow exudative nephritis, nor is it 
merely a modification of it; from the very outset it is a different 
form of inflammation. In the kidneys of persons who have been sick 
only a few days, the characteristic lesions are already evident. Pro- 
52 



658 THE URINARY APPARATUS. 

ductive nephritis is governed by the same law as that which belongs 
to productive inflammation in other parts of the body — the disposition 
of the inflammation to continue as a subacute and chronic condition. 
It is of importance to recognize that in exudative nephritis the lesions 
are temporal, and after their subsidence the kidneys return to their 
normal condition, just as the lungs do after a lobar pneumonia. In 
productive nephritis, on the other hand, some of the lesions are per- 
manent, the kidneys can never return to their normal condition, just 
as in an interstitial pneumonia the lung never gets rid of the new 
connective tissue. 

Post-scarlatinal nephritis is nearly always of the productive form. 
Nephritis complicating diphtheria or developed during pregnancy is 
ver}* frequently of this type. A primary nephritis in a person over 
twelve years old, if of subacute form, is almost invariably a produc- 
tive nephritis. On the other hand, this form of nephritis very sel- 
dom complicates any of the infectious diseases except scarlatina and 
diphtheria. 

These facts assist very much in making the diagnosis between the 
two forms of acute nephritis. It is easy to remember that post-scar- 
latinal nephritis and primary nephritis of subacute type are nearly 
always of the productive form; and that nephritis with diphtheria 
and pregnancy is often of the productive form; while acute nephritis 
under all other conditions is regularly of the exudative form. 

CHRONIC CONGESTION OF THE KIDNEYS. 

There are a number of morbid conditions which interfere with 
the circulation of the blood in the aortic system in such a way that 
the blood accumulates in the veins and is diminished in the arteries. 
The most common of these conditions are : chronic inflammation of 
the aortic and mitral valves, dilatation of the heart, aneurism of the 
arch of the aorta, pulmonary emphysema, and large accumulations 
of fluid in the pleural cavities. , 

In pulmonary emphysema the disturbances of circulation are con- 
fined to the cases in which there is obstruction to the passage of blood 
through the lungs, dilatation and hypertrophy of the right veiitricle, 
and then venous congestion of the aortic system. More or less 
dropsy is regularly developed at about the same time as the conges- 
tion of the kidneys. 

Large accumulations of fluid in the pleural cavities, if they re- 
main for any length of time, may produce well-marked chronic con- 
gestion. 

By far the most common cause of chronic congestion of the kid- 
neys is disease of the heart. So long as a heart with chronic endo- 






THE URINARY APPARATUS. 659 

carditis, or myocarditis, or dilatation, is able, in spite of its dam- 
aged state, to carry on the circulation fairly well, no secondary 
changes in the kidneys are produced. But as soon as the blood ac- 
cumulates in the veins to auy considerable extent the kidneys may 
suffer. One of three things regularly happens to them: either 
chronic congestion, or chronic degeneration, or chronic nephritis is 
developed. It is also necessary to remember that chronic endocar- 
ditis and chronic nephritis often exist in the same person, although 
neither one of them is secondary to the other. 

The kidneys are of medium size, or rather large. Their weight 
is increased, somewhat out of proportion to the increase in size. The 
color is dark-red, the consistence is very hard, the surfaces are 
smooth, the capsules are not adherent. The congestion is most 
marked in the veins of the pyramids; these contain an increased 
quantity of blood, and are often dilated. The capillaries of the cor- 
tex are also congested, but it is rather exceptional to find them 
dilated. The epithelium of the convoluted tubes is swollen, and the 
separate cells of which it is composed are more evident. Or, instead 
of this, the epithelium is much flattened so that the lumen of the tube 
is larger. 

The most constant and characteristic change is in the glomeruli. 
The capillaries which make up the glomerulus are dilated, with more 
or less thickening of their walls. This change in the glomeruli is 
usually, if not always, present and persists, even if the congestion 
is succeeded by a true nephritis. 

While the congestion often persists up to the time of the patient's 
death, it may, instead of this, be followed by a chronic nephritis. If 
that is the case the specific gravity of the urine falls and the excre- 
tion of urea is diminished. The nephritis follows the anatomical 
type of a chronic nephritis without exudation, but the dilatation of 
the capillaries of the gomeruli persists. 

CHRONIC DEGENERATION OF THE KIDNEY. 

{Chronic Bright' s Disease; Chronic Parenchymatous Nephritis; 

Fatty Kidney.) 

The same mechanical obstructions to the circulation — heart 
disease, pleuritic effusions, etc. — which produce chronic congestion, 
can, instead of this, produce chronic degeneration of the kidney. 

It is said that anaemia of the kidneys produces degeneration of 
the renal epithelium. Experiments upon animals show that this 
view is possible. It may be that the degeneration of the kidneys 
seen in old and feeble persons is due to a diminished blood supply, 
but we can hardly speak with certainty on this point. Chronic 



660 THE URINARY APPARATUS. 

diseases, such as phthisis and cancer, are followed by chronic degen- 
eration of the kidneys. There is a group of cases in which, although 
the health of the patients is not good, it is not easy to fix on a defi- 
nite cause for the chronic degeneration. Apparently, many of the 
authors who describe a "chronic parenchymatous nephritis" include 
under this head both chronic degeneration and chronic nephritis. 
The matter is further complicated by the fact that kidneys may be in 
the condition of chronic degeneration for some time, and then become 
further altered by a chronic nephritis with exudation, and by waxy 
degeneration of the glomeruli. 

If the degeneration follows heart disease the kidneys are large, 
and together may weigh from sixteen to twenty ounces. Their sur- 
faces are smooth; the cortical portion is thickened, of pink or white 
color, the pyramids are red. The gross appearance is that of the so- 
called large white kidney. The epithelium of the cortex tubes is 
swollen and coarsely granular. The capillaries of the glomeruli are 
dilated, with more or less thickening of their walls. The veins in 
the pyramids are congested. There are no changes in the stroma, 
or in the arteries. 

If the degeneration follow phthisis, cancer, or any wasting dis- 
ease, the kidneys are usually large, with a white or yellowish cortex. 
There are no changes except in the cortex tubes. In these the 
epithelial cells are either coarsely granular, or infiltrated with fat. 

If the degeneration occur in old people, or without discoverable 
cause, the kidneys may be either large and white, or of the size and 
appearance of a normal kidney, or small and red. There are the 
same degenerative changes in the epithelium of the cortex tubes, 
with no lesions in the stroma or the glomeruli. 

CHRONIC PRODUCTIVE (OR DIFFUSE) NEPHRITIS WITH EXUDATION. 

(Chronic Bright* s Disease; Chronic Parenchymatous Nephritis; 
Chronic Glomerulo- Nephritis; Waxy Kidney; Large White 
Kidney; Chronic Diffuse Nephritis; Chronic Desquamative 
Nephritis.) 

This is a chronic inflammation of the kidney attended with a. 
growth of new connective tissue in the stroma, permanent changes 
in the glomeruli, degeneration of the renal epithelium, exudation 
from the blood vessels, and sometimes changes in the walls of the 
arteries. 

It has been customary to hold that in these kidneys the primary 
and most important changes are in the renal epithelium, while in 
another set of kidneys the primary and important changes are in the 



THE URINARY APPARATUS. 661 

stroma. In other words, that the cases of chronic nephritis can be 
divided into two classes — parenchymatous nephritis and interstitial 
nephritis. 

I (Delafield) do not think that this classification is supported by 
facts. 

In all the forms of chronic nephritis changes are to be found in 
the renal epithelium, the glomeruli, and the stroma. Whether the 
changes in the stroma, the glomeruli, or the epithelium are the more 
marked makes no difference in the clinical symptoms. But the 
presence or absence of exudation from the renal bloodvessels does 
correspond to a marked difference in the symptoms. The existence of 
the exudation from the renal vessels is easily shown by the presence 
of serum albumin in the urine. In this way we readily distinguish 
two forms of chronic nephritis, one with exudation and one without. 

The way of looking at the matter, then, is this : 

We find after death from chronic nephritis a great many varieties 
in the gross appearance of the kidneys. Some are large, some are 
small, some are red, some are white, etc. There is no regular corre- 
spondence between these different gross appearances of the kidneys 
and the clinical symptoms. 

We find in these same kidnej^s changes in the renal epithelium, 
in the stroma, in the glomeruli, and in the arteries. Sometimes one, 
sometimes the other of these elements of the kidneys is the most 
changed. There is no regular correspondence between the predomi- 
nance of the changes in one of the kidney elements over the other 
and the clinical symptoms. 

The easiest working scheme is to admit that in chronic nephritis 
all the elements of the kidney are more or less changed, but that the 
cases vary as to whether there is or is not an exudation of serum 
from the blood vessels. The presence or absence of such an exuda- 
tion does correspond to a well-marked difference in the clinical symp- 
toms. 

In the present state of our knowledge and for clinical purposes, 
we divide all the cases of nephritis into two classes, chronic nephritis 
with exudation and chronic nephritis without exudation. 

It is admitted that it is eas3 T to divide up these kidneys according 
to their anatomical changes, into a number of fairly well-marked 
classes. But as this division does not correspond to clinical divisions 
it is valueless for clinical purposes. 

Although it is convenient to describe two forms of chronic ne- 
phritis — one with much albuminuria and dropsy, and one with little 
or no albuminuria, or dropsy — yet it must be remembered that these 
are not separate lesions of the kidneys, but varieties of the same 
lesion. For in all these kidneys two changes are constant — produc- 



6Q2 



THE URINARY APPARATUS. 



five inflammation of the glomeruli and stroma, and degeneration of 
the renal epithelium. The only real difference between the kidneys is 
whether, besides the growth of new tissue and degeneration of renal 
epithelium, there is or is not an exudation of serum from the blood- 
vessels of the kidneys. 

In speaking of the exudation of serum from the vessels and 
its presence in the urine, we speak of it as it occurs during the 
whole course of the disease, and not as it occurs for short periods. 
We mean that in an exudative chronic nephritis there is usually a 
large quantity of albumin in the urine, but that there may be periods 
during which the albumin diminishes or entirely disappears. In the 
same way, in a non-exudative nephritis there may be periods during 
which albumin is present in considerable quantities. Generally 
speaking, the character of the clinical symptoms will vary with the 
presence or absence of the albumin. 

A considerable number of cases of chronic nephritis follow an 
attack of acute or subacute productive nephritis. The conditions of 
chronic congestion and chronic degeneration of the kidney are not 
infrequently followed by a true nephritis. 

Syphilis, chronic tubercular inflammation of any part of the body, 
chronic endocarditis, and chronic suppurative inflammations are often 
complicated with chronic nephritis. 

It is very difficult to find a satisfactory cause for the primary 
cases. There are man} 7- of these, especially in young and middle-aged 
adults. The nephritis is developed in a slow, insidious way in per- 
sons whose previous health had been good, and in whom no exciting 
cause is discoverable. 

Gross Appearance of the Kidney. — There is considerable vari- 
ety in the gross appearance of the kidneys. The types which I 
(Delafield) have seen most frequently are as follows : 

1. Large white kidneys, weighing together sixteen ounces or 
more, the capsule adherent or not, the surface smooth or nodular, the 
cortex thick and white, the pyramids large and red. 

2. Large mottled kidneys. These resemble the large white kid- 
neys in every respect except that the cortex, instead of being white* 
is mottled in a variety of ways with white, yellow, red, and gray. 

3. Kidneys which resemble types one and two, but are not en- 
larged, the kidneys together not weighing over nine ounces. 

4. Small kidneys, weighing together not more than five ounces,, 
the capsules adherent or not, the surfaces nodular, the cortex thin, 
atrophied, white, the pyramids rather large and red. These kidneys 
belong to persons who have had symptoms of kidney disease for many 
years, with periods of apparent recovery. 

5. Kidneys which have the ordinary appearance and consistence 



THE URINARY APPARATUS. 663 

of the chronic congestion due to heart disease, but in addition the 
capsules are adherent and the surfaces finely nodular. 

6. Kidneys of different sizes — large, medium-sized, and small, 
with adherent capsules and nodular surfaces. The cortex is gra} T , or 
gray mottled with red. The kidneys do not look at all like the large 
white kidneys. This is a type of frequent occurrence. 

7. Kidneys which in their size, color, and general appearance are 




Fig. 319.— Chronic Nephritis with Exudation. 
Cortex with flattened epithelium and containing coagulated matter. 



hardly to be distinguished from normal kidneys, except that their 
capsules are adherent. 

8. Kidneys of small size, weighing together not more than four 
ounces, with adherent capsules. The cortex is atrophied, red, and ir- 
regular. These kidneys are found in persons who have given symp- 
toms of kidney disease for a number of years. 

It might naturally be supposed that such marked differences in 
the gross appearance of the kidneys would correspond to equally 
marked differences in the clinical histories and minute lesions. 



664 



THE URINARY APPARATUS. 



This, however, is not the case. The clinical histories are practically 
interchangeable, and the minute lesions are essentially the same. 

Microscopical Appearances. — If we make vertical sections of 
the cortex of all these kidneys, no matter what their size or color, we 
get with a low magnifying power the same general picture. Instead 
of the uniform and orderly arrangement of tubes and glomeruli which 
we see in the normal kidney, the tubes seem to be obliterated in some 
places and dilated in others. There is a growth of fibro-cellular 




Fig. 320.— Chronic Nephritis with Exudation. 
A glomerulus, showing growth of the tuft cells. 

tissue in regular wedges, in irregular patches, or diffuse between the 
tubules. 

If we examine the different constituents of the kidney in detail 
we find: 

The tubes are in some places of normal size, in some places atro- 
phied, in some places dilated. The atrophied tubes are in the patches 
of new connective tissue. The dilated tubes are not very large, nor 
do they form cysts. 






THE URINARY APPARATUS. 



665 



The epithelium of the tubes is in some places merely flattened. 
These tubes are empty, or contain coagulated matter, casts, and red 
and white blood cells. In other tubes the epithelium is more or less 
swollen, sometimes so much so as to completely fill the tubes. In 
still other tubes the epithelial cells are swollen, their reticulum is 
very coarse with large meshes, and they are infiltrated with fat. 
The kidneys vary as to which of these changes in the epithelium 
predominates, but all of them may be found in the same kidney. 







Fig. 321. — Chronic Nephritis with Exudation. 
Glomerulus showing a growth of the tuft cells. 



The new connective tissue is in the form of wedge-shaped masses 
in the cortex which follow the line of the straight arteries and veins, 
or it is in irregular masses, or it is arranged diffusely so as to sepa- 
rate the tubes from each other. The longer the nephritis lasts, the 
greater is the quantity of new connective tissue. The relative pro- 
portion of basement substance and cells and the density of the base- 
ment substance vary in the different kidneys. The new tissue is well 
supplied with blood vessels. 



666 



THE URINARY APPARATUS. 



The glomeruli are changed in several different ways: 

1. They resemble the glomeruli in acute exudative nephritis. 
They are large, the convolutions of the capillaries are seen with 
difficulty, there is a very great increase in the number of the cells 
which cover the capillaries, but these new cells are not of large size. 
We also see glomeruli, which apparently have been of this type, small 
and atrophied. 

2. There is an increase not only in the number, but also in the 




Fig. 322.— Chronic Nephritis, with Exudation. 
Glomerulus showing a growth of capsule cells. 



size, of the cells which cover the capillaries. These cells are so large 
that they project outward from the surface of the glomerulus. There 
is also an increase in the size and number of the cells within the 
capillaries. These glomeruli are found in all stages of atrophy. 

3. The capillaries are changed in the same way by a growth of 
large cells on their outer surfaces and within them. In addition there 
is a very extensive cell-growth beginning in the cells which line the 
capsule. The mass of new cells produced in this way may be so 



THE URINARY APPARATUS. 



667 



great as to compress the capillaries (Fig. 322) . The glomeruli also 
become atrophied, the capillaries are shrunken, and the capsule cells 
changed into connective tissue. 

4. If chronic congestion of the kidneys is followed by chronic 
nephritis, the dilatation of the capillaries due to the congestion con- 
tinues, and there is added an increase in the size and number of the 
cells which cover the capillaries. 

5. The walls of the capillaries are the seat of waxy degeneration, 
while the cells which cover them are increased in size and number 
(Fig. 323). 




Fig. 323.— Waxy Degeneration op Tuft Capillaries. 
a, the tuft is completely transformed into a waxy mass; b, portions of tuft wax}-; c, tuft ca- 
pillaries normal; d, convoluted tubule with disintegrating epithelium. 



6. Besides the atrophied glomeruli already described, there are 
others which are small and shrunken, with comparatively little new 
growth of cells. 

The arteries are not infrequently much altered by inflammatory 
changes. There is a growth of cells and basement substances from 
the inner surface of the artery which obstructs its lumen ; or there is 
a thickening of each of the three coats of the artery; or all the coats 
of the artery are thickened and converted into a uniform mass of 
dense connective tissue; or the wall of the artery undergoes waxy 
degeneration. 



668 



THE URINARY APPARATUS. 



CHRONIC PRODUCTIVE NEPHRITIS WITHOUT EXUDATION. 

{Chronic Bright' s Disease; Cirrhosis of the Kidney; Granular 
Degeneration; Interstitial Nephritis; Chronic Indurative 
Nephritis; The Arteriosclerotic Kidney.) 

While this form of nephritis is especially common in persons over 
forty-five years old, it is by no means rare in young adults, and is 
occasionally seen in children. 




Fig. 324.— Chronic Nephritis without Exudation. 
Atrophied glomerulus. 

It seems to be caused by chronic alcoholism, lead poisoning, gout, 
and by the same conditions as those which cause emphysema, endo- 
carditis, and cirrhosis of the liver. It follows chronic congestion of 
the kidney, hydro-nephrosis, and chronic pyelitis. 

The larger number of the affected organs are found after death to 
be diminished in size; the two kidneys together may not weigh more 
than two ounces. The capsules are adherent; the surfaces of the 



THE URINARY APPARATUS. 



669 



kidneys are roughened or nodular, the cortex is thin and of a red or 
gray color. 

A considerable number of these kidneys, however, do not differ 
in their size or appearance from normal kidneys, except that their 
capsules are adherent and their surfaces roughened. 

Occasionally the kidneys are large, weighing together from 16 to 
32 ounces, with smooth or nodular surfaces, and a cortex of red, 
gray, or white color. 




>v 






Fig. 325.— Chronic Nephritis without Exudation. 
Showing an atrophied glomerulus. 



If the nephritis follows chronic congestion, the kidneys remain 
hard, but the cortex becomes thinned, the capsules adherent, and the 
surface roughened. 

There is a growth of new connective tissue in the cortex and also 
in the pyramids, which becomes more and more extensive as the 
disease goes on. In the cortex the new tissue follows the distribution 
of the normal subcapsular areas of connective tissue, is in the form 



670 



THE URINARY APPARATUS. 



of irregular masses, or is distributed diffusely between the tubes. In 
the pyramids the growth of new connective tissue is diffuse. 

The tubes, both in the cortex and pyramids, undergo marked 
changes. Those included in the masses of connective tissue are 
diminished in size, their epithelium is flattened, some contain cast 
matter, many are obliterated. The tubes between the masses of new 




Fig. 326. 



-Chronic Nephritis without Exudation. 
An atrophied glomerulus. 



connective tissue are more or less dilated ; their epithelium is flat- 
tened, cuboidal, swollen, degenerated, or fatty. The dilatation of 
the tubes may reach such a point as to form cysts of some size, which 
contain fluid, or coagulated matter. These cysts follow the lines of 
systems of tubes, or are situated near the capsules. 

Of the glomeruli a certain number remain of normal size, but 
with the tuft cells swollen or multiplied. Many others are found in 
all stages of atrophy and of change into connective tissue (Figs. 
324 and 325). The atrophy seems to depend partly on the growth of 






TH3 URINARY APPARATUS. 671 

tuft cells and intra-capillary cells, partly on the thickening of the cap- 
sules, partly on the occlusion of the arteries. If the chronic nephritis 
follow chronic congestion of the kidneys the glomeruli remain large, 
with an increased growth of tuft cells, or they become atrophied, but 
with the dilatation of the capillaries still evident. The capillaries 
of the glomeruli may be the seat of waxy degeneration (Fig. 326). 
The arteries exhibit the same changes as have already been described 
in speaking of chronic exudative nephritis. 

SUPPURATIVE NEPHRITIS. 

Suppurative inflammation in the kidne}' may follow injuries to 
the organ, the lodgment in its vessels of infectious emboli, and may 
accompany p}*elitis and cystitis. 

1. Suppurative Nephritis from Injury. — Gunshot wounds, in- 
cised or punctured wounds, falls, blows, and kicks are the ordinary 
traumatic causes. If the injury be a very severe one it usually causes 
the death of the patient in a short time; if it is less severe, suppura- 
tive inflammation is developed. The inflammatory process may be 
diffuse, so that nearly the whole of one or of both kidneys is converted 
into a soft mass composed of pus, blood, and broken-down tissue; or 
it is circumscribed and one or more abscesses are formed in the 
kidney. 

2. Abscesses. — In pyaemia and in malignant endocarditis small 
infectious emboli find their way into the arteries of the kidneys and 
produce necrosis of small areas of tissue, with surrounding zones of 
suppurative inflammation. The entire kidney is enlarged and con- 
gested, and is dotted with little white foci surrounded by red zones. 
The foci are formed by an infiltration of pus cells between the tubes, 
with more or less degeneration of kidney tissue. Sometimes ab- 
scesses of one or both kidneys are met with which have existed for a 
long time and for which no cause can be discovered. After death the 
kidney may be changed into a sac of pus surrounded by fibrous 
tissue. The pelvis and calyces may be dilated and their walls thick- 
ened. The connective tissue around the kidney, and its capsule, 
ma} 7 be also thickened. Suppurating sinuses may extend from the 
kidney into the surrounding soft parts. 

Whatever the form in which it may manifest itself, suppurative 
inflammation of the kidney may be induced by some one or combina- 
tion of the pyogenic micro-organisms which may lodge within it 
under favorable conditions. 

Thus Streptococcus pyogenes, Staphlococcus pyogenes, Bacillus 
coli communis; the pneumococcus, the typhoid bacillus, and others 
may be found in the suppurative foci. Sometimes, however, espe- 



672 



THE URINARY APPARATUS. 



cially in the more chronic processes, the technical procedures at our 
command fail to reveal the presence of micro-organisms. 

When the suppurative inflammation is consecutive to similar pro- 
cesses in the bladder or ureters the processes are usually due to the 
same infective agent (see page 684). 

Suppurative Pyelitis is often associated with suppuration of the 
kidney substance on the one hand, and on the other hand, and more 
frequently, with a similar process in the bladder or ureters, or both 
on the other. But it may occur by itself. It is incited by the same 
micro-organisms as are concerned in the induction of the associated 
lesions in the kidney and bladder. In the latter case, it is most often 
the Bacillus coli communis, the Streptococcus pyogenes, and Staphy- 
lococcus pyogenes which are concerned. 

The mucous membrane of the pelvis may be congested, thicker 
and more opaque than normal, and coated with pus or with patches 
of fibrin. The presence of pelvic calculi is to be regarded as a predis- 
posing rather than as a direct inciting agent in suppurative pyelitis. 

SUPPURATIVE URETERITIS. 

The conditions under which suppurative inflammation of the 
ureter occurs are similar, as is the general appearance of its mucous 
membrane, to these just indicated in the pelvis. 



SUPPURATIVE PYELONEPHRITIS WITH CYSTITIS. 

("Surgical Kidney") 

In this grouping of lesions, which is usually initiated by the 
inflammation of the bladder, the affection of the kidneys is usually 
bilateral. The suppurative areas in the kidney may be in the form 
of small abscesses scattered through the kidneys, or in the form of 
elongated whitish streaks or wedges between the tubules. The 
purulent foci are often surrounded by a red zone of congestion. 

The kidney tissue in the vicinity of the abscesses may be necrotic, 
the outlines of the cells being preserved but their nuclei absent or not 
revealed by the usual staining agents (see Fig. 68). 

The infective agent may traverse the ureters in the passing from 
the inflamed bladder to the kidneys without leaving the mucous 
membrane of the ureter intact. 



CHRONIC PYELO-NEPHRITIS. 

Chronic cystitis or calculi in the pelvis of the kidneys may set up 



THE URINARY APPARATUS. 673 

a chronic inflammation which involves both the pelvis and calyces 
and the kidney tissue. The mucous membrane of the pelvis and 
calyces is thickened, the epithelial layer is changed, there is a growth 
of granulation tissue beneath the epithelium, and there may be little 
polypoid outgrowths. The surface of the mucous membrane is coated 
with pus or fibrin, or the cavity of the pelvis is dilated and distended 
with purulent serum. 

The kidney itself is the seat of a chronic interstitial inflamma- 
tion with the production of new connective tissue, and sometimes of 
pus, with obliteration of the renal tubules. 

TUBERCULOUS NEPHRITIS. 

This lesion is usually, though not always, associated with tuber- 
cular inflammation in other parts of the genito-urinary tract. 

It is usually unilateral, occurring most frequently on the left side. 
The process may commence in the kidney or in some other part of 
the genito-urinary tract. If only one kidney is involved the other is 
apt to become the seat of chronic diffuse nephritis with waxy de- 
generation of the walls of the arteries. The tubercular inflamma- 
tion may occur in a kidney already the seat of chronic inflammatory 
changes. 

The lesion is apt to begin in the mucous membrane of the pelvis 
and calyces, and extends from thence first to the pyramidal and after- 
ward to the cortical portion of the kidneys. In the mucous mem- 
brane of the pelvis and calyces there is a growth of granulation 
tissue studded with tubercle granula in the stroma, while the epithe- 
lial cells proliferate, become deformed, and desquamate. This pro- 
cess is often rapidly succeeded by cheesy degeneration of all the in- 
flammatory products. 

In the kidney there is the same production of granulation tissue 
and tubercle granula, which soon undergo cheesy degeneration, the 
degeneration involving the adjacent kidney tissue. In addition to 
this there is in the rest of the kidney chronic interstitial or suppura- 
tive inflammation. So the entire kidney is enlarged, portions are in 
the condition of cheesy degeneration or have sloughed away, while 
the rest of the kidney is dense and hard. Or, if suppuration takes 
place, the kidney is hollowed out into cavities filled with cheesy mat- 
ter and pus. 

Sometimes the process comes to a standstill, and then the cheesy 
portions are infiltrated with salts of lime. 

EMBOLISM AND THROMBOSIS. 

Acute and chronic endocarditis affecting the left side of the heart, 
and chronic endarteritis of the aorta, frequently result in the forma- 
53 






674 THE URINARY APPARATUS. 

tion of vegetations, portions of which become detached and lodged as 
emboli in the branches of the renal artery. 

The occlusion of an artery in this way produces in the kidneys 
wedge-shaped infarctions, varying in their size with the size of the 
obstructed artery. The infarction loses the natural red color of the 
kidney and becomes first yellow and then white. The renal epithe- 
lium degenerates and disappears, the tubes become collapsed and 
shrunken ; around the infarction is a zone of congestion and of infil- 
tration with pus cells. After this the infarction becomes shrunken, 
dense, and changed into connective tissue. The kidney is then left 
deformed by the cicatricial depressions and contractions. It is pos- 
sible, however, for the infarction to become gangrenous, or to be 
surrounded by a zone of purulent infiltration, and break down so as 
to form an abscess. Rarely the infarctions are of the hemorrhagic 
variety. 

Embolism of the trunk of the renal artery produces complete ne- 
crosis of the kidney. 

Infectious emboli are small and produce little purulent foci (see 
above). 

Thrombosis of the renal vein and its branches may occur in pa- 
tients suffering from chronic Bright's disease. ' It can also be pro- 
duced by tumors pressing on the veins, by thrombi of: the vena 
cava, and occurs as a primary lesion dependent on the general con- 
dition of the patient. 

HYDRONEPHROSIS. 

Dilatation of the pelvis and calyces of the kidneys is found as a 
congenital condition. In some cases other malformations, such as 
club-foot, hare-lip, and imperforate anus, are also present. The pel- 
ves and calyces of both kidneys, and the ureters, are distended with 
urine ; the bladder is also distended and its wall may be hypertro- 
phied. The urethra may be closed, or no obstruction can be demon- 
strated. In these latter cases it is supposed that there does exist 
some membranous obstruction, which is broken by the probe or 
catheter used to explore the urethra. 

In adult life hydronephrosis is produced by mechanical obstruc- 
tion of the urethra or ureters, due to inflammation, tumors, or 
calculi. According to the position of the obstruction, either one or 
both kidneys are involved. 

The pelvis and calyces are dilated, sometimes enormously, and 
filled with urine alone or urine mixed with pus. The kidney tissue 
is flattened and thinned over the distended cavities. Its texture may 

1 Moxon, Trans. Lond. Path. Society, 1870, p. 248. 



THE URINARY APPARATUS. 



0?5 



remain unchanged, or there may be developed suppurative pyelo- 
nephritis or chronic diffuse nephritis. 

THE CYSTIC KIDNEY. 

Cysts are formed in the kidneys, both during intra-uterine and 
extra-uterine life. 

The congenital cystic kidney is a very remarkable pathological 
condition. Either one or both kidneys are enormously enlarged and 
converted into a mass of cysts. The cysts are of all sizes and are 
separated from each other by fibrous septa or compressed kidney tis- 




Fig. 327. — Cysts of Kidney — Chronio Nephritis. 

sue. They contain a clear yellow, acid fluid holding in solution 
the urinary salts. Or the fluid is turbid and brown, and contains 
blood, uric acid crystals, and cholesterin. The cysts are lined with 
a single layer of flat, polygonal cells. They seem to be formed by a 
dilatation of the tubules and of the capsules of the Malpighian bodies. 
As causes for such dilatations are found obliteration of the tubes in 
the papillae, and stenosis of the pelvis, ureters, bladder, or urethra. 
Other congenital malformations are often associated with this one. ' 
In adult life we find three varieties of cystic kidney : 
1. In kidneys which are otherwise normal there are one or more 



Virch., Ges. Abhandl. 



676 



THE URINARY APPARATUS. 



cysts filled with clear or "brown serum or colloid matter. These 
cysts do not appear to interfere at all with the function of the kid- 
neys. 

2. In chronic diffuse nephritis, especially in the atrophic form, 
groups of tubes are dilated. Apparently one or more of the larger 
tubes in the pyramids is obstructed, and this causes dilatation of a 
corresponding group of tubes. Such a dilatation may be moderate 
in size, or it may form cysts visible to the naked eye. 

3. Both kidneys are very much enlarged and converted into a 
mass of cysts containing clear or colored serum or colloid matter. 
The nature of these cysts is uncertain. It is possible that they are 
congenital. They are sometimes associated with similar cysts in the 
liver. They seem to produce no renal symptoms until shortly before 
the patient's death, unless chronic nephritis also exists, and then 
there are the ordinary symptoms of chronic Bright's disease. 



PERINEPHRITIS. 

The loose connective tissue which is situated around and beneath 
the kidney may become the seat of suppurative inflammation, and in 
this way abscesses of considerable size are formed. 

Such a perinephritis may be either secondary or primary. The 
secondary cases are due to extension of the inflammation from ab- 
scesses in the vicinity, such as are formed with caries of the spine, 
pelvic cellulitis, puerperal parametritis, perityphlitis, and suppura- 
tive nephritis. 

The primary cases occur after exposure to cold, after contusions 
over the lumbar region, and after great muscular exertion ; or no 
cause can be discovered. 

Complicating cases occur in the course of typhus and typhoid 
fevers and of small-pox. 

Most of the reported cases have been in persons between the ages 
of twenty. and forty years. Less frequently children and older per- 
sons are affected. 

In the idiopathic cases the connective tissue behind the kidney 
seems to be the point of origin of the inflammatory process, and it is 
here that the pus first collects. After the abscess has formed the 
suppuration extends and the pus burrows in different directions : 
backward through the muscles ; downward into the iliac fossa, the 
perineum, the bladder, the scrotum, or the vagina ; forward into 
the peritoneal cavity or the colon ; upward through the diaphragm. 

The kidney itself is simply compressed by the abscess, or its tis- 
sue becomes involved in the suppurative inflammation. 



THE URINARY APPARATUS. 677 



RENAL CALCULI. 



In the kidneys of new-born children, from the first to the four- 
teenth day after birth, the large tubes of the pyramids often con- 
tain small, brownish, rounded bodies composed of the urates of am- 
monium and sodium. Similar masses may also be present in the 
calyces and pelves. In still-born children these masses are usually 
absent. The carbonate and phosphate of lime may be deposited in 
the tubes of the pyramids, in the form of white linear masses, in the 
kidneys of old persons and of those who have suffered from destruc- 
tive diseases of the bones. 

Urate of soda in the form of acicular crystals is deposited both in 
the tubes and stroma of the kidneys of gouty persons. 

Concretions of the urinary salts are often formed in the pelves of 
the kidneys. They may remain there as rounded masses, or they 
may attain a large size and be moulded into the shape of the pelvis 
and calyces. Smaller calculi may pass into the ureter and either 
become impacted there or pass through it into the bladder. The 
most common form of calculus is that composed of uric acid. But 
they may also be formed of uric acid with a shell of oxalate of lime, 
or of oxalate of lime alone, or of the phosphates, or of cystin. 

The most serious result of the presence of these calculi is the oc- 
clusion of the ureters or the production of pyelo-nephritis. 

TUMORS. 

Fibroma. — Small, hard, white fibrous nodules are frequently 
found in the pyramids. They are of no special importance. They 
may be mistaken for miliary tubercles. Large fibromata are very 
rare. 1 

Lipoma. — Small fatty tumors are found in the cortex of the kid- 
ney just beneath the capsule. They are composed of fully devel- 
oped fat tissue. The fat is developed in the stroma so as to replace 
the kidney tissue. 2 

Papilloma. — Villous tumors, formed of tufts of connective tissue 
covered with epithelium, may grow from the mucous membrane of 
the pelvis. 3 A peculiar form of papillary and cystic growth of the 
ureter is described. 4 

Myxosarcoma. — Large tumors may grow from the pelvis of the 
kidney. They are not simple myxomata, but are composed of mu- 
cous tissue, fat, and sarcomatous tissue. 

1 Wilks, Trans. Lond. Path. Soc., xx. 

2 For bibliography of fat tumors of the kidney consult TJlvich, Ziegler's Beitr. 
-z. path. Anat.; Bd. xviii., p. 603. 

3 Trans. Lond. Path. Soc, 1870, p. 239. 
4 Virch. Arch., Bd. lxvi., p. 139. 



678 THE URINARY APPARATUS. 

Myoma. — Small tumors composed of smooth muse alar fibres and 
of round cells are found in the cortex close to the capsule. 

A tumor composed of striated muscle and round cells is described 
by Cohnheim. 1 

A tumor composed partly of smooth muscle, partly of striped 
muscle, and partly of sarcomatous tissue is described by Eberth. 2 

Angioma cavernosum occurs in the form of small nodules situ- 
ated in the cortex. 

Lymphoma. — Small white tumors composed of tissue like that of 
the lymphatic glands are found in cases of leukaemia and pseudo- 



& % & %/& ' J A @ 6' -Arts 

aol/-© ..--, a \ ■ a 
5 ^ ;/// : „» ' . ; # ' 5e ' 




M 



© „ a 



/:■*-•** www-. --- 




Fig. 328.— Adenoma of the Kidney. 
Papillary form. 

leukaemia. Less frequently they are found with typhoid fever, scar- 
let fever, and diphtheria. 

Adenoma. — This form of tumor is situated in the cortex of the 
kidney and may invade the pyramidal portion also. Usually there is 
only a single tumor, but sometimes two or more, or they may even 
occur in both kidneys. They vary in size ; some are not larger than 
a pea, others are as large as a hen's egg. They are of rounded form, 
of whitish color, and separated by a capsule from the kidney tissue. 
The tumors are most frequent in persons over forty years of age. 

1 Virch. Arch., Bd. lxv., p. 64. 
2 Ibid., Bd. lv., p. 518. 



THE URINARY APPARATUS. 679 

There are two principal varieties of these tumors, the papillary 
and the alveolar, which are, however, closely related. 

1. The Papillary Adenoma. — There are cavities of different sizes, 
from the walls of which spring branching tufts covered with cylin- 
drical or cuboidal epithelium (Fig. 328). These tufts nearly fill the 
cavities. 

2. The Alveolar Adenoma. — There is a connective-tissue frame- 
work enclosing small round, oval^ or tubular alveoli, lined or filled 
with cells (Fig. 329). 

The cells are usually large and may be cylindrical, cuboidal, or 
polyhedral, and may be pigmented in a manner similar to the cells 
of the adrenals. 






-■'-- -- 'f/ ^ a- 



V; « & g> 



£a 






«" :-,^. 



3^-b ? **>/•*&? #*V* *JJ% i.^^ ^ 



W-*t -'^ >-fe 






Fig. 329.— Adenoma of the Kidney. 
Glandular form. 



Fatty degeneration of the epithelium may be excessive and glyco- 
gen may form in the cells. In these tumors the stroma may be 
present in considerable quantity, or the blood vessels may form con- 
spicuous features, or a cystic distention of the alveoli may occur. 
Large areas in these tumors may become necrotic. 

Many of these tumors appear to have developed from adrenal cells 
estray in the kidneys. They may form metastases. 

The relationship between true adenoma of the kidney, adenomata 
which appear to develop from strayed adrenal elements, and similar 
tumors which are regarded by some observers as endotheliomata or 



680 THE URINARY APPARATUS. 

endothelial sarcomata, and certain forms of angio-sarcoma, is not yet 
altogether clear. 1 

Carcinoma. — Besides secondary carcinoma of the kidney there is 
also a primary form. Our knowledge of this has been much ob- 
scured by confounding with it adenomata and sarcomata. 

There seems to be, however, a real epithelial growth, originating 
in the kidney tubules, which forms tumors of large size and malig- 
nant character. 

Sarcoma. — Tumors formed of connective-tissue cells may origi- 
nate either in the pelvis of the kidney or in the kidney itself. They 
form tumors of large size and malignant character. Those which 
grow from the pelvis are usually myxo-sarcomata. Those which 
originate in the kidney tissue reach a large size and are soft and 
hsemorrhagic. Their stroma forms irregular alveoli filled with small 
round cells. 

PARASITES. 

Echinococcus, in its ordinary form of mother and daughter cysts, 
is sometimes found in the kidney. The cysts may open into the pel- 
vis of the kidney, into the pleura, or through the wall of the abdomen. 

Cysticercus cellidosaz is of very rare occurrence. 

Pentastomum denticulatum has been seen once by E. Wagner. 

Filaria sanguinis hominis is found in the arteries, veins, lym- 
phatics, and stroma. 

Strongylus gigas has been found several times in the pelvis of 
the kidney. 

THE URINARY BLADDER. 
MALFORMATIONS. 

Exstroversion of the bladder is one of the most frequent mal- 
formations, and may occur in either sex. It presents several varie- 
ties : 

1. The umbilicus is lower down than usual, the pubic bones are 
not united at the symphysis, the pelvis is wider and shallower than 
it should be. Between the umbilicus and pubes the abdominal wall 
is wanting. In its place is a projecting, ovoid mass of mucous mem- 
brane, in which may be seen the openings of the ureters. The penis 
is usually rudimentary ; the urethra is an open fissure (epispadias) ; 
the clitoris may be separated into two halves. The ureters usually 

1 Consult Paoli, Ziegler's Beitr. z. path. Anat. , Bd. viii., p. 140; Askanazy, 
ibid., Bd. xiv., p. 33, 1893 ; v. Kahlden, ibid., Bd. xv., p. 626 ; Sudeck, Vircli. Arcli., 
and Ulrich, Ziegler's Beitr. z. path. Anat., Bd. xviii. , p. 589, 1895 ; Lubarsch, 
Virch. Arch., Bd. cxxxv., p. 149. 



THE URINARY APPARATUS. 681 

open normally ; sometimes their openings are displaced or are multi- 
ple. They may be dilated. 

2. There may be a fissure in the abdominal wall, filled up by 
the perfectly formed bladder. 

3. The umbilicus may be well formed, and there is a portion of 
abdominal wall between it and the exstrophied bladder. 

4. The external genitals and urethra may be well formed, and the 
symphysis pubis united, while only the bladder is fissured. 

5. The genitals, urethra, and symphysis may be well formed, the 
bladder closed except at the upper part of its anterior wall. The 
bladder is entirely or in part inverted and pushed through the open- 
ing in the abdominal wall. 

The Urachus normally remains as a very small canal, five to 
seven cm. long, with a small opening into the bladder, or entirely 
closf i at that point. If there is a congenital obstruction to the flow 
of ur ne through the urethra, the urachus may remain open and the 
urine pass through it. Or the bladder may present, even in the adult, 
a slender distention reaching close to the umbilicus as the result of a 
persistent urachus. 1 

Absence of the Bladder is of rare occurrence. The bladder may 
be very small, the urine passing almost directly into the urethra. 
The bladder may be separated into an upper and a lower portion by 
a circular constriction. It may be completely divided by a vertical 
septum into two lateral portions. Diverticula of the wall of the 
bladder are sometimes found in new-born children. Partial or com- 
plete closure of the neck of the bladder may occur. This may lead 
to hydronephrosis, or the urine may be discharged through the open 
urachus. 

CHANGES IN SIZE AND POSITION. 

Dilatation. — This may be general or partial, leading to the 
formation of diverticula. 

General dilatation of the bladder is produced by the accumulation 
of urine in consequence of some mechanical obstacle to its escape, or 
of paralysis of the muscular walls of the organ. The dilatation is 
usually uniform and may be very great, so that the bladder may 
reach to the umbilicus. If the walls of the bladder are paralyzed, or 
the obstruction occurs suddenly or is complete, the wall of the blad- 
der is thinned. When an incomplete obstruction exists for some 
time the walls of the bladder are apt to hypertrophy, so that, al- 
though the bladder is larger than normal, the walls may not only be 
of the usual thickness, but even very much thicker. In the foetus 

*My, Trans. N. Y. Path. Soc, 1893, p. 64. 



6S2 



THE URINARY APPARATUS. 



dilatation of the bladder may reach such a size as to interfere with 
delivery. 

The retained urine in dilated bladders is liable to decomposition, 
leading to inflammation or gangrene of the mucous membrane. 

Diverticula of the bladder may be produced by the pouching-out 
of circumscribed portions of the wall of the bladder, the wall of the 
pouch containing all the layers of the bladder wall. More frequently, 
however, they are produced by a protrusion of the mucous membrane 
between hypertrophied bundles of muscle fibre. They may be very 
small, or they may be as large as a child's head. They may com- 
municate with the bladder by a large or a small opening. The de- 
composition of stagnant urine in diverticula is apt to induce inflam- 
mation. Calculi may be formed in them or may slip into them from 
the bladder. 

Hypertrophy of the muscular coat of the bladder is usually pro- 
duced by mechanical obstructions to the outflow of urine, such as 
stricture of the urethra, enlarged prostate, calculi, new growths, etc. 
The muscular coat is thickened uniformly or assumes a trabeculated 
appearance. The organ retains its normal capacity, or is dilated, or 
becomes smaller. The mucous membrane is frequently the seat of 
chronic or acute inflammation. Dilatation of the ureters and hydro- 
nephrosis frequently accompany this condition. 

Hernice of the bladder sometimes accompany intestinal hernise 
through the inguinal and crural canals and the foramen ovale. The 
changes in position of the bladder, produced by displacements of 
the vagina and uterus, will be mentioned with the lesions of those 
organs. 

In the female the base of the bladder may press downward, caus- 
ing protrusion of the vaginal wall (vaginal cystocele) ; or there 
may be inversion and prolapse of bladder through the dilated 
urethra. 

RUPTURE — PERFORATION. 

Penetrating wounds of the bladder may permit escape of urine 
into the abdominal cavity, or infiltration into the surrounding con- 
nective tissue, or permanent fistulae. Such wounds are always seri- 
ous and frequently fatal, owing chiefly to the severe and often 
gangrenous inflammation which decomposing urine sets up in the 
connective tissue, or to the peritonitis induced by the same cause. 

Rupture of the bladder may be produced by severe blows and 
falls when the bladder contains urine. More rarely rupture takes 
place from overdistention. Death may occur from rupture of the 
bladder with escape of urine into the peritoneal cavity, without evi- 
dences of peritonitis. 



THE URINARY APPARATUS. 683 

Perforations of the bladder are produced by ulceration and 
gangrene, by abscesses from without, and by cancerous ulceration 
from the adjoining organs. Fractures of the pelvic bones may pro- 
duce laceration of the bladder. Perforations of the bladder may 
lead to the establishment of flstulae, communicating with the rectum, 
vagina, uterus, or opening externally. 

DISTURBANCES OP CIRCULATION. 

Hypercemia. — Aside from active hypersemia of the mucous mem- 
brane in acute inflammation, the bladder is not infrequently the seat 
of chronic congestion from obstruction to the venous circulation. 
Under these conditions there may be chronic catarrhal inflamma- 
tion, or a marked dilatation of the veins (vesical haemorrhoids) , 
which may give rise to haemorrhage or to obstruction of the opening 
of the ureters. 

Hcemor? % hage.— Extensive haemorrhages into the bladder are com- 
monly due to injury or to the presence of calculi or tumois. Small 
haemorrhages into the substance of the mucous membrane may ac- 
company inflammation, the haemorrhagic diathesis, scurvy, purpura, 
small-pox, etc. If the haemorrhage is considerable and occurs rapidly 
in an empty bladder, a clot is apt to form ; but when the blood mixes 
with urine as it is extravasated it more commonly remains liquid and 
is discharged as a reddish-brown fluid. 

INFLAMMATION. 

Acute Cystitis.— This may be incited by the presence of urine 
which has decomposed under the influence of bacteria; by cantha- 
rides or other drugs; by the presence of foreign bodies and calculi; 
or it may be due to an extension of gonorrhceal urethritis or vagi- 
nitis; or it may occur without assignable cause. The mucous mem- 
brane is swollen and congested, although these alterations may not 
be very evident after death. The surfaces may be coated with mucus 
containing red blood cells and pus. The epithelium is apt to be 
loosened and in some places peeled off, so that superficial or deep ul- 
ceration may occur. We may find mixed with the urine in the 
organ shreds of mucus, pus cells, epithelial cells of various shapes, 
usually more or less swollen and granular, or fragments of such cells; 
red blood cells and bacteria. Resolution may occur from acute ca- 
tarrhal cystitis, but it very frequently assumes a chronic character. 

Chronic Cystitis. — In this form the mucous membrane may be 
swollen, succulent, grayish, or mottled with spots of congestion or 
extravasation, and covered with a layer of mucus and pus. Micro- 
scopically the membrane may be more or less infiltrated with pus 



684 THE URINARY APPARATUS. 

cells, and pus may be constantly produced and thrown off into the 
urine. Later the mucous membrane may become thickened either 
diffusely or in the form of tufts or polypi. In some cases it becomes 
atrophied. Owing to decomposition of the haemoglobin in the extra- 
vasated blood the mucosa may become pigmented, brown, or slate- 
colored. The mucous membrane frequently becomes eroded, espe- 
cially on the most elevated portions, or deep ulcerations may occur. 
The muscular coats may become paralyzed and the bladder dilated; 
or the submucosa or the muscularis, or both, may become hypertro- 
phiecl. The mucous membrane may become encrusted with urinary 
salts. 

In another class of cases the inflammation assumes a more intense 
and necrotic character. Larger and smaller shreds and patches of 
the mucosa die, become brown or gray in color, loosen or peel off, 
and become mixed with the urine and exudations. The gangrenous 
process may extend to all the coats of the bladder, so that perforation 
and fatal peritonitis may occur. The gangrenous form of cystitis is 
more apt to occur in paralytics. In still another class of cases the 
inflammation assumes a suppurative character. The submucosa, the 
intermuscular connective tissue, and the adjacent parts become infil- 
trated with pus, either diffusely or in the form of larger and smaller 
abscesses, which may open externally or internally, forming deep 
ulcers. In all these cases the inflammation may extend to the ureters 
and kidneys; it may skip the ureters and involve the kidneys. 

The small nodules of lymphoid tissue in the mucous membrane 
of the bladder, especially near the neck, may become enlarged and 
prominent in cystitis, and may then be mistaken for miliary tubercles 
(nodular cystitis).' 

Croupous Inflammation. — In connection with any of the above 
lesions the mucous membrane of the bladder may be covered, in 
patches or sometimes over a considerable portion of its surface, with 
a layer of fibrin, either granular or fibrillar, enclosing pus and epi- 
thelial cells and bacteria. The mucosa may be infiltrated with 
fibrin. 

This form of inflammation may occur in connection with severe 
infectious diseases — measles, diphtheria, scarlatina, typhoid fever; 
in connection with similar inflammation of the external genitals, in 
puerperal fever, noma, and sometimes in the presence of foreign 
bodies. It is rarely an idiopathic disease. 

Various forms of bacteria have been found in the urine in connec- 
tion with the various phases of inflammation of the bladder. 

Aside from the tubercle bacillus which is always concerned with 

1 Alexander, Journal Cutaneous and Nervous Diseases, July, 1893. 



THE URINARY APPARATUS. 685 

tuberculous lesions, the most common micro-organisms are the Bacil- 
lus coli communis, Streptococcus pyogenes, and Staphylococcus pyo- 
genes and Bacillus proteus. Many other forms are of occasional 
occurrence. 

While the exact significance of the germs named in connection 
with cystitis is not yet fully clear, there is much reason to attribute 
serious importance especially to the Bacillus coli communis. 1 

Tuberculous Inflammation. — This disease commences by the for- 
mation of miliary tubercles in the mucous membrane of the bladder. 
By the coalescence of the tubercles and the degeneration of tissue 
about them, ulcers are formed, and it is most frequently in the ulcer- 
ative stage that the lesion is seen. The ulcers, which may be large 
or small, are usually most abundant at the base of the organ. Their 
edges may be cheesy, and miliary tubercles in greater or smaller 
numbers are usually found in the mucosa about them. Not infre- 
quently large shreds of tissue are loosened and cast off. The mucosa 
about the ulcers is apt to bo infiltrated with small spheroidal cells. 
Tubercle bacilli are present in many of the tubercles and in the edges 
and base of the ulcers. They may also be found in the urine, and 
are then of diagnostic significance. Catarrhal inflammation is a 
very constant accompaniment of this lesion. Tubercular cystitis 
may occur in connection with tubercular inflammation of the lungs, 
intestines, or of the kidney, uterus, prostate, etc. 

TUMORS. 

Fibromata have been described, occurring as small nodular tu- 
mors in the submucosa, but they are rare. 

Aside from the polypoid thickenings of the mucosa occurring in 
chronic cystitis, soft vascular papillomata are of frequent occur- 
rence. These tumors vary in size from that of a pea to that of a 
pigeon's egg or larger. They consist of a fibrous, often very vascu- 
lar stroma, and are covered on the surface with numerous small, 
closely set, villous projections, over which are irregular layers of 
elongated or cylindrical cells. These tumors are very liable to bleed, 
are often accompanied by vesical catarrh, and may be covered by a 
precipitate of urinary salts. The epithelium is liable to peel off from 
the surface of the villi and appear in the urine. Sarcoma of the 
bladder has been described. 

Carcinoma. — Carcinoma of the bladder is most frequently sec- 
ondary, and is then rarely due to metastasis, but usually to an ex- 

1 Consult Schmidt and Aschoff, "Die Pyelonephritis, " Jena, 1893; also Barlow, 
Arch. f. Dermatologie u. Syphilis, 1893, p. 355 ; also Melchior, "Cystitis and Urinary 
Infection," 1895 (bibliography). 



686 



THE URINARY APPARATUS. 



tension of the growth from neighboring parts, as the uterus, vagina, 
or rectum. 

Primary carcinoma of the bladder may occur : 

1. As a diffuse scirrhous infiltration of the entire wall of the 
bladder, usually with ulcerations of its inner surface. 

2. As a circumscribed nodule which grows inward and out- 
ward, ulcerating on its inner surface, and sometimes producing per- 
forations. 

3. As villous or papillomatous growth. The tumor grows 
from one or more points of the inner surface of the bladder. It is 



rfpl 




m 



n 



■n> 



Fig. 330.— Papilloma of the Bladder. 






^&^- 



formed of tubular follicles lined with cylindrical epithelium, and, 
on its inner free surface, of tufts covered with cylindrical epithe- 
lium. The new growth may involve the entire thickness of the wall 
of the bladder. 

4. A few cases of carcinoma have been described in which the 
stroma contained a varying quantity of smooth muscle tissue. * 

Cysts. — Dermoid cysts of the wall of the bladder have been de- 
scribed, but are rare. Small cysts with serous contents sometimes 
occur in the mucous membrane ; a part of them, at least, are be- 
lieved to be due to faulty embryonal development. 

1 The literature of tumors of the bladder may be found in Stein's " Study of the 
Tumors of the Bladder," 1881. 



THE URINARY APPARATUS. 687 

PARASITES, ETC. 

Among the animal parasites occasionally found in the bladder 
may be mentioned Echinococcus, Distoma haematobium, Filaria 
sanguinis, Ascarides, and Oxyuriases. 

A great variety of foreign bodies may be found in the bladder, 
particularly in the female. If their stay is long they are apt to be- 
come encrusted with urinary salts. 

CALCULI. 

Vesical calculi may occur singly or in great numbers, and vary 
greatly in size, ranging from small, sand-like particles up to masses 
four or five inches in diameter, but the usual range is from the size 
of a pea to that of a hen's egg. They are usually oval, spheroidal, 
or elongated ; or, when several are present, they are apt to be 
faceted. The surface may be smooth or rough. They are usually 
more or less distinctly lamellated, and are frequently formed around 
a central body called a nucleus, which may either be formed of 
urinary salts or some foreign body. Their most common constitu- 
ents are phosphates, uric acid and urates, and calcium oxalate, 
or various combinations of these. 

Uric Acid Calculi. — These are the most common of vesical cal- 
culi. In the form of small brownish-red, crystalline aggregations 
they may be passed as " gravel." The larger uric acid calculi are 
not commonly of very great size, are frequently finely nodulated on 
the surface, but may be smooth. The color varies from light yellow 
to dark reddish-brown ; they are usually dense and lamellated. 

Calculi formed of Urates. — Calculi composed of pure urates 
are rare, these salts being more commonly combined with uric acid 
and the phosphates to form the complex calculi. Sodium urate, in 
the form of small spined, more or less globular crystalline masses, 
forms one of the varieties of " gravel." 

Phosphatic Calculi. — Pure calcium phosphate calculi are, rarely, 
found as whitish, usually smooth, and small lamellated concretions. 

Mixed or Triple Phosphate calculi are common, and frequently 
attain large size. These calculi are sometimes pure, but the deposit 
is more frequently associated with other salts, either as encrusting or 
intercalated lamellae. Triple phosphate calculi are usually rough on 
the surface, of grayish-white color, lamellated, and frequently very 
friable. 

Small gray or white, hard, and usually smooth calculi of pure 
calcium carbonate occur rarely. Calcium carbonate is sometimes 
passed as gravel in the form of minute spheroidal bodies, either 
singly or in clusters. 

Calcium Oxalate calculi (mulberry calculi) are comparatively 



688 



THE URINARY APPARATUS. 



common, either pure or in combination with uric acid or the phos- 
phates. Calcium oxalate may occur in the form of very small, hard, 
smooth concretions, or as larger, heavy, hard, finely or coarsely 
nodulated brown or blackish lamellated masses. The nucleus or 
some of the lamellae, or both, are often composed of uric acid. 

Cystin Calculi are usually ovoidal in shape, of waxy consistence, 
of clear or brownish or greenish-yellow color, with mammillated 
surface and crystalline fracture. Cystin may be associated in a 
variety of ways with other calculi. 

Xanthin Calculi, which are very rare, are usually of moderate 
size, smooth, of a cinnamon or cinnabar-red color, lamellated, and 
oval or flattened in shape. 

Solid masses of fibrin and blood sometimes occur in the bladder, 
and may exist as independent structures, or form nuclei for the de- 
posit of urinary salts. 

For a detailed account of calculi, the conditions under which 
they form, modes of analysis, etc., we refer to special works on this 
subject. 

THE URETHRA. 
CONGENITAL MALFORMATIONS. 

Some of the malformations of the urethra are described with 
those of the penis. 

The urethra may be impervious or may open at the root of the 
penis. More commonly there is partial obliteration or stricture of 
some part of the canal. 

The entire urethra may be dilated into a sac full of urine. 

There may be a canal on the dorsum of the penis, formed by the 
fusion of the spermatic cords, and opening in the glans above the 
urethra. 

There may be two or more openings of the urethra. 

The canal may be dislocated so as to open in the inguinal re- 
gion. 

A number of cases have been reported in which a valve in the 
urethra has produced hypertrophy of the bladder, dilatation of the 
ureters, and hydronephrosis. 1 

Owing to its narrowness, greater length, and peculiar connec- 
tions with the internal generative organs, the male urethra is much 
more liable to disease than the female. 



CHANGES IN SIZE AND POSITION. 

Dilatation of the urethra may be produced by strictures, or by 
1 Virch. Arch., Bd. xlix., p. 348. 



THE URINARY APPARATUS. 68 d 

calculi or other bodies fixed in its lumen. The dilatations are fusi- 
form or sacculated in shape, and may reach the size of an orange or 
be even larger. 

Strictures of the urethra are usually produced by inflammation of 
its walls. 

The stricture may be temporary, produced by a diffuse inflamma- 
tory swelling of the mucous membrane, or by the raising of the re- 
laxed membrane into a fold or pocket. 

Permanent strictures are produced by structural changes in the 
walls of the urethra. 

1. The mucous membrane and submucous tissue are left hard 
and unyielding by the preceding inflammation. Subsequently the 
new fibrous tissue contracts and narrows the canal. 

2. Ulceration of the mucous membrane leaves cicatricial tissue, 
which contracts, and also produces adhesions and bands of fibrous 
tissue. 

3. There is fibrous induration of the corpus spongiosum and con- 
sequent constriction of the urethra. 

The most frequent position of strictures is at the junction of the 
membranous and spongy portions of the urethra, or close to this 
point. They also occur at the fossa navicularis and the meatus, but 
frequently in the prostatic portion. There may be one stricture or 
several. The consequences of stricture are dilatation of the urethra, 
the bladder, the ureters, and hydronephrosis ; inflammation and ul- 
ceration of the urethra behind the stricture, with perforation, infil- 
tration of urine, or the formation of fistula?. 1 

The urethra may also be obstructed by folds of the mucous mem- 
brane ; by muscular valves at the neck of the bladder ; by wounds ; 
by polypi and swollen glands ; by new growths ; by changes in the 
prostate and perineum ; by calculi, mucus, blood, and echinococci 
coming from the bladder ; by foreign bodies introduced from with- 
out. 

Prolapse and inversion of the mucous membrane is seen in young 
girls and women in rare cases. There is a bluish-red swelling, from 
the size of a pea to that of a walnut, at the meatus. In the male 
invagination of the mucous membrane of the urethra has been seen 
after injuries of the perineum 

WOUNDS — RUPTURE — PERFORATION. 

Wounds of the urethra are produced in many ways, but most 
commonly by catheters and bougies. The wounds may cicatrize, or 

1 For literature of stricture of urethra, and plates illustrating several forms, see 
article by Dittel in Pitha and Billroth's "Handbuch der allg. Chirurgie," Bd. iii., 
Abth. 3. 

54 









690 THE URINARY APPARATUS. 

there may be infiltration of urine or the formation of fistulse or false 
passages. 

Ruptures of the urethra are produced by severe contusions and 
by fracture of the pelvic bones. Extravasations of blood and urine, 
and gangrenous inflammation of the surrounding soft parts, are the 
ordinary results. 

Ulceration and perforation of tne urethra may lead to the forma- 
tion of fistulse, which open in various directions through the skin. 

INFLAMMATION. 

Catarrhal Urethritis may be simple and due to the action of 
chemical irritants, to the extension to the urethra of inflammation 
from other parts, and to unknown causes ; but it is most frequently 
due to the action of the gonorrhoeal poison. In its acute form it in- 
volves either a portion or the whole of the urethra. The mucous 
membrane is red, swollen, and covered with muco-pus. The inflam- 
mation may extend to the fibrous wall of the urethra, the corpora 
spongiosa and cavernosa. This may result in the formation of new 
connective tissue or of abscesses, especially near the fossa navicula- 
ris. The inflammation may also extend to the bladder, the glands 
of Cowper, the prostate, the spermatic cord, and the testicles. The 
inguinal glands also may be swollen and inflamed, and the lymphatic 
vessels on the dorsum of the penis may be involved in the same pro- 
cess. 

Chronic inflammation of the urethra may exist for a long time 
with the production of a muco-purulent exudation, but without the 
occurrence of marked structural lesions. In other cases it leads to 
ulceration, to fibrous induration of the wall of the canal, to indura- 
tion and swelling of the mucous follicles, to polypoid thickenings of 
the mucous membrane. 

The exudation in gonorrhoeal inflammation of the mucous mem- 
branes, not only of the urethra but also of the vagina and of the eye, 
constantly contains, in greater or less numbers, a form of micrococ- 
cus which is said by some observers — although this is denied by 
others — to present characteristic morphological characters. 

The Micrococcus gonorrhoeae — called gonococcus — which is spher- 
oidal or ovoidal in shape, usually occurs in pairs or in groups of four 
or more, and may be contained in the pus cells (Fig. 80) or lie on 
their surfaces or free in the fluid. The pus cells sometimes contain 
very large numbers of the micrococci. 

The gonococcus may be stained by drying the exudation on a 
cover glass and using Gram's method. 

For details as to the biology of the gonococcus see page 206. 



THE URINARY APPARATUS. 691 

Croupous Inflammation is sometimes seen in children. Fibrin- 
ous casts of a small or large portion of the canal may be formed. 

Syphilitic Ulcers may be situated at the meatus or as far back 
as the fossa navicularis. They are apt to produce strictures. 

Tubercular Inflammation rarely occurs in the mucous mem- 
brane of the urethra in connection with tubercular inflammation of 
the bladder, prostate, or testicles. 

TUMORS. 

Aside from the polypoid outgrowths from the mucous membrane 
of the urethra as the result of chronic inflammation, fibrous polyps 
may occur congenitally, or polyps containing glandular structures 
or cysts rarely occur. Carcinoma may occur as a result of local 
extension from adjacent organs or metastasis from the bladder. 
Cysts may occur in the mucous membrane as a result of the dilata- 
tion of the mucous glands. Circumscribed masses of dilated veins 
occasionally occur in the urethra, forming the so-called urethral 
hemorrhoids. 

The sinus pocularis may be dilated in children by the retention 
of its secretion, so as to form a tumor which may obstruct the exit 
of urine, cause hypertrophy of the bladder and dilatation of the 
ureters. 



THE OEGAl^S OF GE^ERATIOW. 



FEMALE GENERATIVE ORGANS. 
THE VULVA. 

MALFORMATIONS. 

The external genitals may be entirely absent or imperfectly de- 
veloped. The fissure between the labia may be unformed, or the la- 
bia may grow together, with or without obstruction of the urethra. 
The clitoris and nymphae may be abnormally large, or the nymphs© 
may be increased in number. The clitoris may be abnormally long, 
resembling a penis ; at the same time the vagina is narrow, the ute- 
rus small and undeveloped or malformed ; the ovaries small, some- 
times situated in the labia ; the mammae small, and the body of a 
masculine character. Such cases are sometimes called pseudo-her- 
maphrodites. The clitoris may be perforated by the urethra or may 
be cleft and apparently double. 

The hymen frequently exhibits various anomalies. It may be 
entirely absent. The opening may be very large or in unusual pla- 
ces ; there may be several openings ; the free edge may be beset 
with papillary projections ; there may be no opening at all. 1 

HEMORRHAGE, HYPEREMIA, ETC. 

Haemorrhage may take place from wounds or ulcers of the vulva, 
but the most important form of haemorrhage is that which occurs in 
the connective tissue of the labia majora. This is produced during 
labor or from external injury. One of the labia may be swollen and 
distended by the extravasated blood until it is as large as a child's 
head. The blood may be gradually absorbed, or it may decompose 
with suppuration or gangrene of the surrounding tissue. The puru- 

1 For description and illustrations of anomalies of the hymen, which may be use- 
ful for medico -le^al purposes, see Court fs " Diseases of Uterus, Ovaries, Fallopian 
Tubes," Trans, by McLaren, 1883, p. 90. 



THE ORGANS OF GENERATION. 693 

lent matter may escape through the skin and the patient recover, or 
the suppuration may extend into the pelvis and cause death. 

A varicose condition of the veins of the labia is not infrequent. 
CEdema may occur in acute form in pregnant and puerperal women, 
and may terminate in suppuration or gangrene. CEdema of the la- 
bia majora frequently accompanies disturbances of the venous cir- 
culation, as in certain heart and lung diseases ; or it may occur in 
chronic diffuse nephritis or other ^wasting diseases, or as a result of 
thrombosis or other disturbances of circulation in the uterine or peri- 
vaginal venous plexuses. This may be excessive, leading to the 
transudation of fluid through the skin, to the formation of vesicles, 
to superficial erosion, or even to gangrene. 

INFLAMMATION. 

The skin, mucous membrane, connective tissue, and glands of 
the vulva may be the seat of inflammation. Acute catarrh of the 
mucous membrane may be caused by a variety of irritating influ- 
ences, but is most frequently due to gonorrheal infection. The 
mucous membrane is swollen and red and covered with a muco-pu- 
rulent exudation. The labia may be swollen, the glands of Bartho- 
lin are liable to be involved, and abscesses of the labia may be de- 
veloped. Chronic catarrhal inflammation may lead to superficial or 
deep ulceration of the mucous membrane, or to papillary outgrowths, 
or to thickening of the labia. Suppurative inflammation of the tis- 
sue of the labia may occur in connection with a similar process in 
neighboring parts. Erysipelatous inflammation of the skin of the 
vulva is frequent in young children and may cause death. In adults 
it is less common. Inflammation of the vulvo- vaginal glands may 
be acute and produce abscesses, or chronic and produce induration of 
the gland. 

Gangrene may follow erysipelatous inflammation, may occur after 
parturition, may accompany severe exhausting and infectious dis- 
eases, or may occur as an epidemic disease, especially among chil- 
dren. It may be the result of bruises or other injuries. In some 
forms, such as those known as noma and hospital gangrene, the 
destruction of tissue proceeds with extreme rapidity. 

Herpes, eczema, lichen, prurigo, etc., may be found on the skin 
of the vulva. 

Syphilitic inflammation and ulceration are of frequent occurrence 
on the vulva, particularly on the mucous surfaces, and frequently 
lead to considerable destruction of tissue and cicatricial contractions. 

Simple Croupous Inflammation may occur, with or without 
diphtheria and a similar lesion of the fauces or elsewhere, and is fre- 
quently associated with gangrene. 



694 THE ORGANS OF GENERATION. 

Lupus. — This form of inflammation, usually with more or less 
destructive ulceration, occasionally occurs in the vulva. 

TUMORS. 

Fibroma. — Circumscribed fibrous tumors are found in the con- 
nective tissue of the labia, mons veneris, perineum, clitoris, and 
entrance to the vagina. They may attain a large size, and, attached 
only by a pedicle, may hang far down between the legs. The skin 
is usually movable over the surface of these tumors. 

Fibroma diffusum (elephantiasis). — This usually involves the 
clitoris or the labia, or both, and may extend to surrounding parts 
of the skin. It consists essentially of a diffuse hypertrophy of the 
skin and subcutaneous tissue, with or without involvement of the 
papillae and epidermis. The surface may be smooth or rough. 
Sometimes when the new growth is circumscribed, rough or smooth 
polypoid growths, often of large size, are formed. When the papillae 
and epidermis are much involved, larger and smaller cauliflower-like 
excrescences may cover the hypertrophied parts and the surface be 
very rough and scaly. 

Papillomata. — These growths consist of hypertrophied papillae 
covered with thick layers of epithelium. They vary in size from 
that of a pea to that of an apple, and have a cauliflower appearance. 

Syphilitic Condylomata. — In one form, the so-called mucous 
patch, there is an infiltration of the papillary layers of the skin or 
mucous membrane with variously shaped cells and fluid, so that the 
tissue has a gelatinous appearance. In other cases there is an 
hypertrophy of the papillae, so that larger and smaller wart-like ex- 
crescences are formed. This is called the pointed condyloma. 
Lipomata, fibro-myomata, and fibro-sarcomata are of occasional 
occurrence in the vulva. A few cases of melano-sarcoma are re- 
corded. Chondroma of the clitoris has been described. Carcinoma 
of the vulva may be primary, usually in the form of epithelioma of 
the clitoris or labia, or it may be secondary to cancer of the uterus, 
vagina, etc. 

Cysts are found in the connective tissue of the labia majora and 
minora. They are from the size of a pea to that of a child's head. 
They may contain serum, colloid material, purulent or bloody fluid, 
or they may have the characters of dermoid cysts or atheroma cysts. 
Their origin is in many cases obscure. In some cases they are 
doubtless due to dilatation of lymph vessels. Cysts may be formed 
by a stoppage and filling with fluid of the canal of Nuck, or by a dila- 
tation of the ducts or acini of the vulvo-vaginal glands. 



THE ORGANS OF GENERATION, 695 



THE VAGINA, 



MALFORMATIONS. 



The vagina may be entirely absent, and the internal organs of 
generation also absent or imperfectly developed. 

Either the upper or the lower portion of the canal may be absent 
while the remaining portion is present. 

The vagina may be closed by an imperforate hymen or by fibrous 
septa at any part of its canal. The canal may be abnormally small 
without being occluded. 

The vagina may be double, in connection with a double uterus ; 
or. while the uterus is normal, the vagina may be incompletely di- 
vided by a longitudinal septum. 

CHANGES IN SIZE AND POSITION. 

Dilatation of the vagina is produced by tumors, by the prolapsed 
uterus, and by the accumulation of blood and mucus behind con- 
strictions or obliterations of the canal. Lengthening of the vagina 
is produced by any cause which draws the uterus upward. Xar- 
rowing of the vagina is found as a senile change ; is produced by 
tumors and by ulceration of the wall of the canal. Extensive ulcers 
may even cause entire obliteration of the canal. 

Prolapse of the vagina occurs by itself, usually as a result of 
thickening or laxity of its walls, or in connection with prolapse of 
the uterus. As an idiopathic process it usually takes place soon 
after parturition. A larger or smaller portion of the canal is in- 
verted and projects through the vulva. The entire circumference of 
the canal may be inverted and prolapsed, or only the anterior or pos- 
terior wall. The prolapse is at first small, but may afterward grad- 
ually increase in size and may drag down the uterus with it. In 
other cases prolapse of the uterus is the primary lesion, and the 
vagina is inverted by the descent of that organ ; or the body of the 
uterus may retain its normal position, while an hypertrophy and 
lengthening of the cervix alone drag down the vagina. 

Hernia vesico-vaginalis — cystocele — may be either the cause or 
effect of a prolapse of the vagina and uterus. If the cystocele is the 
primary lesion, it begins as a small projection of the wall of the blad- 
der into the anterior part of the vagina. As the urine accumulates 
in this sac it increases in size, projects through the vulva, draws 
down the vagina and the anterior lip of the cervix, and finally the 
entire uterus. If the cystocele is the secondary lesion, it is simply 
produced by the dragging-down of the posterior wall of the bladder 
by the inverted vagina. 



096 THE ORGANS OF GENERATION. 

Hernia intestino-vaginalis. — A portion of the intestines may be- 
come fixed in Douglas' cul-de-sac between the rectum and the uterus. 
This portion of intestine gradually becomes larger, pushes forward 
the posterior wall of the vagina, inverts and fills up that canal, and 
finally projects through the vulva. It may drag with it the pos- 
terior wall of the vagina and the uterus. 

Rectocele vaginalis. — A sac is formed by the projection of the 
anterior wall of the rectum and the posterior wall of the vagina. 
This lesion is of rare occurrence and does not reach a large size. 

When the vagina is prolapsed there is usually an inflammatory 
condition of the lining membrane or a thickening of the epidermis. 

WOUNDS — PERFORATIONS. 

Wounds of the vagina are made by penetrating instruments, by 
forceps and other obstetrical weapons, and by the foetus during 
delivery. Such wounds may heal, may give rise to large haemor- 
rhages, may suppurate, may produce abscesses in the surrounding 
tissues, may leave fistulous openings into the vagina or may cause 
constriction or obliteration of its canal. 

Vesico-vaginal Fistulas are usually produced by injuries from 
instruments or from the foetus during delivery ; less frequently by 
ulceration of the vagina, bladder, or adjacent connective tissue, or 
by abscess in the surrounding parts. The fistulse form an opening 
between either the bladder or the urethra and the vagina. They 
allow the urine to pass into the vagina. Spontaneous cure does not 
take place. 

Recto-vaginal Fistulas are formed in the same way as the last- 
mentioned. They allow the passage of gas or faeces into the vagina. 
They sometimes heal spontaneously. 

INFLAMMATION. 

Catarrhal Inflammation of the vaginal mucous membrane may 
be acute or chronic. It is most frequently caused by gonorrhoeal 
infection, but may be due to local irritation or depend upon general 
causes. It not infrequently occurs in the new-born. In the acute 
form the mucous membrane is swollen and frequently covered with 
a muco-purulent or a purulent exudation. In the chronic form the 
mucous membrane may be swollen, covered with a purulent exuda- 
tion ; there may be an exfoliation of epithelium, shallow or deep ero- 
sions, or ulcers. 

Sometimes large shreds or membranes are cast off from the va- 
gina which consist wholly of exfoliated, flat epithelium (Fig. 331). 
In other cases the mucous membrane is thickened, dense, and some- 






THE ORGANS OF GENERATION. 697 

times pigmented, or it may be roughened, covered with papillae, or it 
may be relaxed and prolapsed. 

Croupous Inflammation may occur after parturition, in dysen- 
tery, in typhus and typhoid fever, diphtheria, scarlatina, measles, 
and other infectious diseases. The mucous membrane is swollen and 
covered with a grayish layer of fibrin and pus. The mucosa and 
submucosa may be infiltrated with fibrin and pus. The infiltrated 
portions of the mucosa and submucosa may die and become gangre - 
nous, and thus deep and extensive ulcers be formed. 

Suppurative Inflammation of the fibro-muscular coat of the 
vagina may occur after injuries or in pregnant and puerperal wo- 
men. Abscesses may be formed which penetrate into the labia or 
into the pelvic connective tissue. In other cases the intense phleg- 



Fig. 331.— Vaginal Epithelium 
A fragment from a large exfoliated mass. 

naonous inflammation may lead to the death and casting-off of por- 
tions of the vaginal wall, or even of the entire wall. 

Gangrene of the vagina may occur as a result of croupous or 
intense suppurative or syphilitic inflammation, or from unknown 
causes. In the form of noma it may be very extensive and rapidly 
destructive. 

Tuberculous and Syphilitic Inflammation, usually leading to 
more or less extensive ulceration, may occur in any part of the 
vagina. Tuberculous inflammation is secondary to tuberculosis of 
other parts. Syphilitic ulcers may heal, sometimes leaving marked 
cicatrices, and sometimes not. 

TUMORS. 

Fibroma, fibro-myoma, sarcoma, myoma Icevicellulare, are of 



698 THE ORGANS OF GENERATION. 

occasional occurrence in the vagina. Myoma striocellulare is of rare 
occurrence. 

Papillomata are of frequent occurrence as a result of chronic 
inflammation. Carcinoma of the vagina is usually secondary to 
cancer of the uterus. It may be primary as a circumscribed nodular 
tumor, or more frequently it occurs in a papillary and ulcerating 
form and often spreads to neighboring parts. 

Cysts. — These are not very common and may be small or as 
large as a hen's egg. They may be lined with flattened epithelium, 
and contain serous or viscid, dark-colored or transparent fluid. 

PARASITES. 

Among the animal parasites Oxyuris and Trichomonas vagina- 
lis are of occasional occurrence. Among the vegetable forms Oidium 
albicans, Leptothrix are occasionally seen, while micrococci and 
various other forms of bacteria are common. Staphylococcus and 
Streptococcus pyogenes have been found many times in the normal 
vagina. The pathogenic significance of the bacteria in the vagina 
is not yet established. 

THE UTEEUS. 
MALFORMATIONS. 

The uterus, up to the third month of intra-uterine life, consists of 
two large cornua, which by the fusion of their lower ends form the 
uterus. 

The uterus, tubes, and vagina may be entirely absent, with or with- 
out absence of the external genitals. Or the uterus alone, or the 
upper part of the vagina also, may be absent. 

The uterus may be only rudimentary while the vagina is normal. 
It then appears as a flattened solid body with solid cornua. Or there 
are two cornua joined at their lower extremities so as to form a small 
double uterus. Or the uterus is represented by a small sac, which 
may or may not communicate with the vagina. Or there is a very 
small uterus, with thin muscular walls and two large cornua. 

Only one of the cornua which should form the uterus may be 
developed while the other is arrested in its growth. The uterus is 
then a long, cylindrical body, terminating above in one tube. On 
the side where the other horn should have been developed there is no 
tube, or only a rudimentary one. Both ovaries are usually present. 

The two cornua may be fully developed, but their lower ends 
remain separated and form a double uterus. An entire separation 
into two distinct uteri and vaginae is very rare. More frequently the 
uterus consists of one body, divided by a septum into two cavities. 






THE ORGANS OF GENERATION. 699 

There are then two cervical portions of the uterus projecting into 
a single vagina, or each into a separate vagina. Or there is only 
a single cervix. The septum in the uterus may be complete or only 
partial. 

We also find abnormal size of the uterus, abnormal flexions ; the 
cervix may be solid or may be closed by the vaginal mucous mem- 
brane. Or the cervix may have an abnormal form with a small 
opening or canal. 1 

CHANGES IN SIZE. 

In the new-born infant the uterus is small, the body flattened, 
the cervix disproportionately large. During childhood the organ 
increases in size, but the body remains small in proportion to the 
cervix. At puberty the shape changes and the body becomes larger. 

At every menstruation the uterus is somewhat swollen and con- 
gested. After pregnancy it does not return to its virgin size, but re- 
mains somewhat larger. In old age it gradually becomes smaller • 
its walls are harder and more fibrous. 

Abnormal Smallness of the uterus is sometimes found as an ar- 
rest of development. The uterus in adult life retains the size and 
shape of that of the infant. It may result, however, from chronic 
endometritis, from repeated pregnancies, from old age, or from 
chronic exhausting diseases. Its cavity may be smaller than nor- 
mal, or distended with mucus. Large myomata sometimes cause 
marked atrophy of the uterine wall. Atrophy of the vaginal portion 
of the uterus is sometimes observed after repeated pregnancies, some- 
times without known cause. Narrowing and obliteration of the 
cavity of the uterus and of the cervix are usually produced by chronic 
inflammation. 

Enlargement of the Uterus may be due to too early develop- 
ment. It is accompanied by abnormally early development of all the 
sexual organs and functions. The uterus may be enlarged in con- 
nection with heart disease, prolapse and abnormal flexions and ver- 
sions, chronic inflammations, repeated pregnancies, myomata, and 
accumulations of blood or mucus in the uterine cavity. Enlarge- 
ment of the vaginal portion may be produced by the above causes, 
and is also found without known cause. One or both lips of the 
cervix may be uniformly increased in size, or they may be lobulated. 

Dilatation of the uterus is produced by accumulations of blood, 
mucus, or pus in consequence of narrowing or obliteration of the cer- 
vix or vagina. The uterine walls may retain their normal thickness, 
be thickened or thinned. The most frequent position of the stenosis 

1 Illustrations of various forms of malformation of the cervix may be found in the 
translation by McLaren of Gourty's " Diseases of the Uterus, Ovaries, etc.," 1883. 



700 THE ORGANS OF GENERATION. 

is the os internum. The retained contents after a time change in 
character, forming a thin, serous fluid — hydrometra — or they may 
be mixed with blood. The dilated uterus is not usually larger than 
an apple, but it sometimes reaches enormous dimensions. If both os 
internum and os externum are closed the cervical cavity may be also 
dilated and the uterus have an hour-glass shape. If the obstruction 
is in the vagina, the uterus and vagina may form a large, flask- 
shaped body, and the line of demarcation between cervix and vagina 
be lost. In some cases the dilatation is confined to the cervix. If 
the obstruction is not complete the retained fluid may escape into 
the vagina and afterward accumulate again. 

Accumulation of menstrual blood in the cavity of the uterus — 
hcematometra — is usually produced by congenital stenosis of the 
cervix or vagina. The dilated uterus may reach an enormous size. 
If the fluid is not evacuated by surgical interference there may be 
either rupture or ulcerative perforation of the uterus. The blood 
may escape into the abdominal cavity, or be shut in by adhesions, or 
perforate into the bladder or intestines. Sometimes the blood passes 
into the Fallopian tubes, dilates them, and escapes through their ab- 
dominal ends. 

CHANGES IN POSITION. 

The body of the uterus may become fixed in an abnormal position, 
while the situation of the cervix is unchanged. The body may be 
bent forward — anteflexion ; backward — retroflexion ; or sideways 
— lateral flexion. The flexion may be slight, or so great that the 
neck and body form an acute angle. Anteflexion is the most com- 
mon variety, and that in which the flexion is greatest. Peritoneal 
adhesions, flaccidity of the uterine walls, particularly after delivery, 
atrophy of the walls, ovarian and other tumors, etc., are the usual 
causes of flexions. 

The Versions of the uterus consist in an abnormal inclination of 
the long axis of the organ to that of the vagina. The uterus may be 
inclined backward, forward, or to one side. 

Retroversion is very much the most common. The fundus uteri 
is directed backward and downward, the cervix forward and up- 
ward. This condition is found in various degrees ; in the highest the 
fundus lies in Douglas' cul-de-sac with the cervix upward, so that the 
axis of the uterus is parallel to that of the vagina, but in a direction 
nearly opposite to the normal one. Abnormal looseness of the ute- 
rine ligaments, abnormally large capacity of the pelvis, hypertrophy 
or tumors of the uterus, and pregnancy during the first four months, 
are some of the more common conditions under which this lesion 
occurs. 

Anteversion. — Inclination of the fundus forward and downward, 



THE ORGANS OF GENERATION. 701 

and of the cervix backward and upward, is not common and sel- 
dom reaches a high degree. It occurs under the same general ex- 
ternal conditions as anteflexion. 

Lateroversion is not very common as a simple lesion, but is not 
infrequently combined with other displacements. It may be pro- 
duced by congenital shortening of one of the broad ligaments, by ad- 
hesions, or by the pressure of tumors. 

The greater degrees of version may produce very grave lesions. 
The urethra and rectum may be compressed. Cystitis, perforation of 
the bladder, dilatation of the ureters and hydronephrosis, and fatal 
obstruction of the bowels may follow. If pregnancy exists abortion 
may take place, or the inverted uterus may be forced through the 
peritoneum and posterior wall of the vagina and project through 
the vulva. In the non-pregnant uterus pressure on the veins and 
consequent chronic inflammation of the organ may follow. 

Prolapsus Uteri consists of a descent of the uterus into the 
vagina. The uterus may be only slightly lowered or it may project 
at the vulva. In complete prolapse we find a tumor projecting 
through the vulva, partly covered by the distended vagina, and pre- 
senting the opening of the os externum near its centre. The blad- 
der and rectum may be drawn down with the vagina or may remain 
in place. The exposed cervix and vagina usually become inflamed 
and sometimes ulcerated, or the mucous membrane may become 
thickened. The lesion is frequently complicated by hypertrophy of 
the cervix. 

Gradual prolapse, which is most frequent, may be due to an in- 
creased weight of the uterus, as in pregnancy, inflammatory enlarge- 
ment, the presence of tumors, etc. ; or to some abnormal condition of 
the uterine supports. It is frequently caused by a vaginal cystocele 
or rectocele. Sudden prolapse is most apt to occur in an enlarged 
uterus or one unduly heavy by reason of tumors connected with it. 
It is most common in subinvolution after parturition. 

Elevation of the uterus is produced by mechanical causes crowd- 
ing or dragging it upward, as adhesions, tumors, etc. The vagina 
is drawn up and lengthened, and the vaginal portion of the cervix 
may be obliterated. 

Inversion of the uterus consists of an invagination of the fun- 
dus. The fundus may be invaginated in the body, the fundus and 
body in the cervix, or the entire organ in the vagina. It usually oc- 
curs when the uterine walls are relaxed, and is very frequently due 
to traction on the placenta during parturition. It may take place 
spontaneously after parturition. It may be produced by intra-ute- 
rine tumors. The mucous membrane of the inverted organ is fre- 
quently inflamed, particularly when the inversion is complete. 



702 THE ORGANS OF GENERATION. 

Hernice of the uterus are rare. Ventral hemice may occur dur- 
ing the latter months of pregnancy, the peritoneum, aponeuroses, 
and skin being forced outward to form a sac in which the uterus 
lies. Crural hernice are produced by the drawing-down of the ute- 
l'us and ovaries into the sac of an intestinal hernia. Inguinal her- 
nia may be produced in the same way or be congenital. Ischiatic 
hernia has been seen. Pregnancy may occur in the uterus while 
situated in a crural or inguinal hernia. 

RUPTURE AND PERFORATION. 

Rupture of the unimpregnated uterus is rare. It may, however, 
occur when the uterine cavity is distended with blood or serum, or in 
connection with large myomata of the uterine walls. 

In the gravid uterus ruptures have been seen in nearly every 
month of pregnancy, but most frequently toward the end. The rup- 
ture may be produced by thinning of the uterine wall by tumors, or 
by violent contusions, or as the result of cicatricial contraction of 
the os. 

The act of parturition is the most frequent cause. Malpositions 
of the foetus, narrowing of the pelvis, protracted labor, thinning of 
the uterine wall from tumors, forcible use of the forceps and other 
instruments, are the ordinary causes. The rupture may be in the 
body of the uterus or the cervix, or both ; it may be large or small ; 
it may extend completely or only partly through the uterine wall. 
The consequences of partial rupture are haemorrhage, gangrenous 
inflammation of the edges of the rupture, peritonitis, and usually 
death. In rare cases the rupture cicatrizes and the patient recov- 
ers. Complete rupture usually causes death in a short time. The 
foetus escapes partly or completely into the abdominal cavity. If 
the patient survives the immediate shock, fatal peritonitis soon en- 
sues. In rare cases the foetus is shut in by adhesions and the pa- 
tient survives. 

Perforations of the uterus may be produced by carcinoma, by 
abscesses in its neighborhood, and by ovarian cysts. 

HYPEREMIA— UTERINE AND PERI-UTERINE HAEMORRHAGE. 

Hijpercemia. — Aside from the active menstrual hyperaenria, the 
uterus may be hypergemic in acute and chronic inflammation, as a re- 
sult of displacement of the organ, and in certain forms of heart dis- 
ease. The organ is usually enlarged, the mucous membrane swol- 
len, and the veins more or less evidently dilated. 

Haemorrhage. — Effusion of blood into the cavity of the uterus 
occurs normally at the menstrual periods. For the abnormalities to 
which this function is subject we refer to works on gynaecology. 




THE ORGANS OF GENERATION. ?03 

Effusions of blood at other than the menstrual periods may be caused 
by mechanical hyperaemia, by haemorrhoids, by acute hyperaeraia, 
by intra-uterine polypi and other tumors, by acute and chronic in- 
flammation, by typhus fever, scurvy, etc., by ulcerating carcinoma, 
by abortions and miscarriages. 

A peculiar form of haemorrhage is the polypoid haematoma, or 
fibrinous polypus of the uterus. It occurs after parturition arid after 
abortions. The portion of the uterine wall where the placenta was 
attached, with or without a portion of retained placenta, forms the 
point of attachment of the pedicle of the polypus. We find a large, 
polypoid, bloody mass firmly attached by a pedicle to the uterine 
wall. The uterus enlarges with the growth of the polypus, the cer- 
vix is dilated, and the thrombus projects into and may even fill up 
the vagina. The formation of such a thrombus is accompanied by 
repeated haemorrhages. 

Haemorrhage in the substance of the uterus occurs in old age. 
The mucous membrane and uterine wall are infiltrated with blood, 
and there is some blood in the uterine cavity. Several cases of hae- 
morrhagic infarction in the cervical portion of the uterus have been 
described. 1 

Peri-uterine or Retro-uterine Hcematocele consists in an accu- 
mulation of blood around the uterus or in Douglas' cul-de-sac. It 
maj' consist of blood extravasated into the abdominal cavity, which 
settles into the pelvis : or, in consequence of local hyperaemia, there 
may be repeated extravasations of blood. In the latter case the local 
peritonitis may produce false membranes, between the layers of 
which haemorrhages take place. A similar condition rarely occurs 
in the male. The haemorrhagic mass may become encapsulated, or 
may soften or suppurate and perforate into the rectum or vagina, or 
may be absorbed, A form of extraperitoneal haematocele is de- 
scribed in which the blood lies between the folds of the broad liga- 
ment. The extravasation may proceed from haemorrhage of any of 
the abdominal viscera or rupture of aneurisms ; from vascular new- 
formed false membranes ; from rupture of the varicose veins of the 
broad kgaments ; from rupture of kaemorrkagic cysts of tke ovaries ; 
from tke Fallopian tubes in tubal pregnancy or in kaematometra ; or 
from general causes, suck as scurvy, purpura, etc. In seme cases 
tke extravasation begins at a menstrual period, and increases at tke 
succeeding periods. 

Ante-uterine Hcematocele is of occasional occurrence, either in 
connection with the retro-uterine form or when the posterior cul-de- 
sac is obliterated. 



1 See Chiari. Praeer med. Woehenschr. , Bd. sxi., ZSo. 1*2. 1896. 



704 



THE ORGANS OF GENERATION. 



INFLAMMATION. 

I. Inflammation of the Unimpregnated Uterus. 

Acute Catarrhal Endometritis. — In this disease, which in its 
lighter grades may leave but little alteration after death, the mucous 
membrane is swollen, hyperaemic, and sometimes the seat of punc- 
tate haemorrhages. The epithelium may desquamate, and the mu- 







■Mm, 



/. '''$ 



i'; 'I'.'..- 



'■^■'-.jis 



Fig. 333. — Chronic Endometritis with the Formation of a Polypoid Outgrowth from the 

Mucous Membrane. 



cosa contain an undue quantity of small spheroidal cells. The sur- 
face is more or less thickly covered with muco-purulent exudation. 
Id severe cases shreds of mucous membrane may be exfoliated. The 
lesion is usually most marked in the mucous membrane of the body, 
but may involve the cervix at the same time, or the cervix alone. 
The body of the uterus may be swollen and hypersemic. In dys- 
menorrhea mernbranacea there may be an expulsion, with more or 
less blood, of membranous masses consisting of fibrin mingled with 
blood and pus cells, or consisting of exfoliated superficial layers of 



THE ORGANS OF GENERATION 



705 



epithelium. This exfoliated epithelium is frequently much flattened 
so as to considerably resemble the vaginal epithelium. When the 
shreds are large the openings of the uterine glands may be seen as 
perforations. Acute catarrhal inflammation of the uterus may be 
due to injury, exposure during menstruation, the gonorrhceal infec- 
tion, local infection with other bacteria, or it may accompany the 
general acute infectious diseases. 

Chronic Endometritis. — This may be a continuation of an acute 
inflammation or begin as a chronic disease. In some of the lesser 
degrees of inflammation we find but slight changes after death. 
The mucous membrane, on the other hand, may be swollen, hyperse- 




Fig. 333.— Adenomatous Hyperplasia of the Uterine Mucous Membrane. 
This section is from a large polypoid outgrowth which protruded from the cervix uteri. 

mic, and covered with muco-puruient exudation. In oither cases 
there is more or less well-marked thickening of the mucous mem- 
brane, which may present a smooth or a rough papillary surface or 
polypoid outgrowths (Fig. 332). Owing to the hypertrophy of the 
uterine glands in this condition, these papillary outgrowths, which 
are not infrequently scraped off by the surgeon, often present the 
appearance of adenomata. This condition is called ''adenomatous 
hyperplasia of the uterine mucous membrane" (see Fig. 333). Some- 
times a thick layer of new-formed, very vascular tissue develops over 
the surface of .the mucous membrane, largely covering in the uterine 
glands (Fig. 334). From the decomposition of extra vasated blood in 
the mucous membrane the latter may be mottled with brown or 



706 



THE ORGANS OF GENERATION. 



black. The glandular elements of the mucosa may be partially or 
almost entirely destroyed. The papillae of the cervix may be hyper- 
trophied, the mucous follicles swollen and their outlets obstructed, 
leading to the formation of the so-called ovula Nabothi. The uter- 
ine Avail becomes flaccid and atrophied, or it may be hypertrophied, 
especially in the cervical portion. Ulceration of the mucous mem- 
brane, especially of the cervix, may occur. Contraction or oblitera- 
tion of the cervical canal may occur. The inflammation may extend 
to the Fallopian tubes or to the vagina. 

Chronic endometritis may exist at any age, but is most common 




— a 



, '■;, ■*■"< ; ; ;^-^,;' 



Fig. 334. -Chronic Endometritis with the Formation of a Thick Layer of New-formed, very 

Vascular Tissue over the Surface of the Mucous Membrane. 

a, uterine muscle tissue; 6, mucous membrane of uterus; c, new-formed vascular tissue. 

after puberty, and is produced by a great variety of causes. It may 
occur in ill-nourished persons or in those suffering from exhausting 
diseases. It may be due to displacements and tumors of the uterus, 
subinvolution, injuries, etc. 

Croupous Endometritis. — This form of inflammation is not very 
common. It occasionally occurs in the puerperal uterus, in acute 
infectious diseases, cholera, typhoid fever, the exanthemata, etc. 
The disease sometimes involves the vulva, vagina, and Fallopian 
tubes. It may co-exist with croupous inflammation of the colon. 

Tuberculous Endometritis. — This usually occurs as part of tuber- 



THE ORGANS OF GENERATION. 707 

culous inflammation of the genito-urinary tract. We find a part or 
the whole of the cavity of the uterus lined with a rough, yellowish 
or gray, cheesy mass, which may deeply involve the muscular walls 
of the organ. At the edges of the ulcerating cheesy areas we may 
find well-defined miliary tubercles, or we may find tubercles scattered 
through the otherwise intact mucosa. The lesions resemble those of 
tuberculous nephritis. 

Syphilitic Endometritis, — The results of this infection are 
usually confined to the cervical portion, and consist of shallow or 
deep ulcerations and condylomata of the mucous membrane ; or there 
may be a diffuse thickening of the mucosa. 

Acute Jletritis is usually the result of acute catarrhal endome- 
tritis. The organ is swollen, succulent, congested ; the mucous 
membrane covered with muco-pus ; the peritoneal coat congested. 
There may be small extravasations of blood in the wall or cavity of 
the uterus. The inflammation, in rare cases, becomes suppurative, 
and abscesses are formed in the uterine wall ; these may perforate 
into the peritoneal cavity or into the rectum. 

Chronic Metritis is the result of an acute metritis or accompanies 
acute or chronic endometritis, and is dependent upon the same con- 
ditions : subinvolution, displacements, tumors, active irritants, etc. 
The uterus is enlarged, the wall congested, thickened, and soft, or, 
owing to the new formation of connective tissue, hard and dense. 
The lesion may be most marked in the body or in the cervical portion. 

Perimetritis. — The peritoneal coat of the uterus may be inflamed, 
with the production of membranous adhesions or of pus. The 
adhesions may be small or very extensive, and, owing to their con- 
tractions, may cause various distortions and displacements of the 
pelvic organs. The inflammation is usually an accompaniment of 
chronic metritis and endometritis. In prostitutes such adhesions 
are of very common occurrence. 

Parametritis. — The connective tissue about the uterus, between 
that organ and the reflexions of the peritoneum, may be the seat of 
suppurative inflammation. It most frequently causes the death of 
the patient, but may result in the formation of dense connective 
tissue about the uterus. 

II. Inflammation of the Pregnant Uterus. 

The forms of inflammation which have just been described may 
attack the pregnant uterus. Catarrhal endometritis may produce 
effusion of serum, extravasations of blood, and abortions. Metritis 
may lead to softening of the uterine wall, so that rupture takes place 
during labor. Perimetritis and parametritis produce adhesions and 
abscesses about the uterus. 



708 THE ORGANS OF GENERATION. 

Puerperal Inflammation. 

For a week or more after delivery we find the inner surface of 
the still dilated uterus rough, especially at the insertion of the pla- 
centa, and covered with blackened, gangrenous-looking shreds of 
blood, mucous membrane, and placenta. This condition is not to be 
mistaken for inflammation. 

As a result of some injury to the uterus or vagina during or after 
delivery, and the action of some infectious material which may 
gain access to the tissues, the puerperal uterus is liable to become 

W0M('h ':"' ' lit 'V' 

m 



-,;' 1 '''"-' 









Fig. 335.— Uterine Phlebitis following Delivery with Retained Placenta. 
Death nine days after delivery. Micrococci in the walls of the inflamed veins stained violet. 

the seat of a series of severe and often destructive inflammatory and 
necrotic changes. These may be confined to the uterus; they may 
induce serious alterations in surrounding parts; they may lead to an 
involvement of the peritoneum, or to pyemia and its accompanying 
lesions in the most distant parts of the body. In one series of cases 
a more or less extensive gangrenous inflammation of the mucous 
membrane and the underlying parts may lead to the casting-off of 
larger and smaller shreds of necrotic tissue and the formation of deep 
and spreading ulcers, which may be accompanied by severe para- 
metritis and fatal peritonitis. This condition may be due to in- 
jury or to the presence of decomposing portions of retained placenta. 
In other cases the inflammation has a croupous character, which may 



THE ORGANS OF GENERATION. 709 

affect the vagina and lead to necrosis and gangrene, ulceration, and 
peritonitis. In connection with either of the above forms of inflam- 
mation, or without them, there may be thrombosis of the uterine 
sinuses, purulent inflammation of the veins, suppuration and ab- 
scess in the uterine wall, suppurative inflammation of the ovaries 
and tubes, and, owing to the generalization of the infectious mate- 
rial, metastatic abscesses in the lungs, spleen, kidneys, etc. Or 
acute pleurisy, ulcerative endocarditis, purulent inflammation of the 
joints, hyperplastic swelling of the spleen and lymph nodes, may fur- 
nish characteristic features of the presence of an acute infectious dis- 
ease. In some cases which rapidly pass to a fatal termination the 
local lesions may be but slightly marked, and general alterations 
characteristic of pyaemia, such as metastatic abscesses, etc., be en- 
tirely wanting. Life seems to be overcome by an acute septic in- 
toxication. 

Micrococci are very constantly present in the exudation, in the 
lymph vessels, veins, and inflamed tissue of the uterus (see Fig. 
335) ; often in enormous quantities in the peritoneal exudation and 
in the metastatic inflammatory foci. There is good reason for be- 
lieving that the destructive local processes are due, in the majority 
of cases, to the presence of the Streptococcus pyogenes, and that the 
general infection in this, as in other forms of septicaemia and pyae- 
mia, is dependent upon the same cause (see Septicaemia). 

ULCERATION AND DEGENERATION. 

Catarrhal, tubercular, and syphilitic ulceration have been 
mentioned above. 

Phagedenic or Corroding Ulcer. — This rare form of ulceration 
usually occurs in old age, without assignable cause. It begins in the 
cervix and gradually extends until it may destroy the greater part 
of the uterus or even invade the bladder and rectum. The ulcer is 
of irregular form ; its base is rough and blackish, its walls indu- 
rated. It should not be confounded with carcinomatous ulcer, which 
it considerably resembles. 

Fatty Degeneration. — This may occur in connection with in- 
flammatory changes, in acute infectious diseases, and in phosphorus 
poisoning. 

Amyloid Degeneration in the uterus is of rare occurrence. It 
may affect the muscle fibres or the walls of the blood vessels. 

TUMORS. 

Fibromata. — Dense nodular fibromata of the uterus are exceed- 
ingly rare, the so-called fibromata being in most cases myomata or 
fibro-myomata. Fibroma papillare, on the other hand, is a com- 

56 



710 THE ORGANS OF GENERATION. 

mon form of growth from the mucous membrane. It consists of a. 
more or less vascular connective-tissue stroma covered with epithe- 
lium. The surface may be smooth or villous. It may contain 
very numerous gland follicles, and then approaches the type of 
adenoma, or even carcinoma. The stroma may be loose and succu- 
lent, and resemble mucous tissue, forming the so-called mucous 
polypi; and these again may contain glandular structures. In any 
of these forms the blood vessels may be abundant and dilated, form- 
ing telangiectatic or cavernous polypi. The adenomatous polypi may 
become cystic from the dilatation of the gland follicles. 

Polypi of the uterus may be multiple or single, small or large. 
Numerous smaller and larger papillary outgrowths from the mucous 
membrane may occur in chronic endometritis. Single polypi may 
grow from the mucosa of the body of the uterus or from the cervix, 
and hang by a long pedicle down into the vagina. 

The large number of glandular structures in many of these chro- 
nic inflammatory, papillary, and polypoid outgrowths (Figs. 332 
and 333) often justifies the name of adenomatous hyperplasia of the 
mucous membrane or of adenomatous papillomata or polyps. 

Syphilitic papillary growths in the form of pointed condylomata 
may form finely papillary, wart-like excrescences of variable size, 
particularly on the cervix. 

Myomata. — These tumors, whose characteristic structural ele- 
ments are smooth muscle cells (see Fig. 137), are the most common of 
uterine tumors and are frequently of no special practical importance, 
but are sometimes of very serious import. They are especially com- 
mon in negroes. They are most frequently composed of both mus- 
cular and fibrous tissue — fibro-myomata — but the relative amount 
of the two kinds of tissue is subject to great variation. They are 
most apt to occur after puberty, and usually in advanced life. They 
may be single or multiple, small or of enormous size ; are usually 
sharply circumscribed, whitish or pink, dense and hard, or some- 
times soft, and present on section interlacing bands or irregular 
masses of glistening tissue. Their favorite situation is in connection 
with the body of the uterus, but they may occur in the cervix or 
in the folds of the broad ligaments. According to their position 
we may distinguish subserous, submucous, and intraparietal forms. 
The subserous myomata grow from the outer muscular layers of 
the uterus in the form of little nodules. As they increase in size 
they may become separated from the uterine wall and remain at- 
tached only by a narrow pedicle or by a little connective tissue. 
They may work their way between the folds of the broad ligament 
until they are at some distance from their point of origin. Some 
authors mention cases in which the tumors became entirely detached . 



THE ORGANS OF GENERATION. 711 

from the uterus and were free in the abdominal cavity. In some 
cases the tumors excite inflammation of the adjacent peritoneum, 
leading to the formation of adhesions or of collections of pus. Cases 
are recorded in which, owing to the atrophy of the pedicle, subserous 
myomata have become completely detached from the uterus and 
were held in place and nourished by peritoneal adhesions. In other 
cases the tumor reaches a large size, but remains firmly attached to 
the uterus. This organ may then be drawn upward, the cervix and 
vagina being elongated and narrowed. The traction may be so great 
that the body of the uterus is entirely separated from the cervix. 
The bladder may also be drawn upward, producing incontinence of 
urine and cystitis. Subserous myomata are very often multiple and 
frequently attain great size. 

The submucous myomata grow from the inner muscular layers 
of the uterine wall. They commence as rounded nodules which lift 
up the mucous membrane. The usual position is the fundus uteri. 
They rarely occur in the cervix. As the tumors increase in size they 
project into the uterine cavity. They then remain continuous with 
the uterine wall over a large area, or are attached by a large or 
small pedicle. They are usually well supplied with vessels. The 
uterus dilates with the growth of the tumor, and its walls may be 
also thickened. The tumor may reach such a size as to entirely fill 
the cavity of the dilated uterus and project through the cervix into 
the vagina. 

The submucous myomata are usually single, although there may 
be at the same time subserous and intraparietal tumors. They are 
frequently soft. If they are of large size and polypoid in form, they 
may project through the cervix and drag down the fundus of the 
uterus, producing inversion. The mucous membrane covering them 
may be atrophied or hyperaemic, with dilated blood vessels, and may 
thus give rise to severe and repeated haemorrhages. Haemorrhage 
may occur in the substance of these tumors. Inflammation, suppu- 
ration, and gangrene may also occur. The surface may be ulcerated. 
In some cases the pedicle of the tumor is destroyed and it is sponta- 
neously expelled. 

The intraparietal myomata grow in the substance of the uterine 
wall, but, if they attain a large size, project beneath the serous or 
the mucous coat. They are found in every part of the uterus, but 
are most frequent in the posterior wall. 

The shape of the uterus is altered in a great variety of ways by 
the presence of these tumors ; its cavity is narrowed, dilated, or 
misshapen ; it undergoes flexion and version in every direction. The 
tumors may sink downward and become attached to the posterior 
wall of the vagina, looking as if they grew from it. They may, 



712 THE ORGANS OF GENERATION. 

without the formation of a pedicle, project into the cavity of the 
uterus, fill it up, and project through the cervix. The uterus is 
dilated, its wall hypertrophied or atrophied. 

The tumors themselves may undergo a variety of secondary altera- 
tions. The muscle fibres may undergo fatty degeneration, and the 
tumor diminish in size, or may even undergo, it is said, entire destruc- 
tion and atrophy. Calcification may occur, converting a part or the 
whole of the tumor into a stony mass. The intraparietal and sub- 
mucous myomata may give rise to profuse haemorrhages ; thay may 
suppurate and become gangrenous. 

Sometimes the tumors or circumscribed portions of them are very 
vascular, constituting the telangiectatic or cavernous variety. 
These tumors, which possess some of the characters of erectile tissue, 
may suddenly change in size from a variation in the amount of blood 
which they contain. 

A very important change which is sometimes found in these 
tumors is the development of cysts in their interior (fibro-cystic tu- 
mors). This sometimes takes place in those tumors which grow out- 
ward beneath the peritoneal coat. We find one or more cavities 
communicating with each other, with rough, trabeculated walls. 
The appearance is more that of cavities than of cysts. There may 
be a number of smaller cavities, or they may fuse to form one large 
one. The fluid contained in the cavities is like synovia, or is mixed 
with blood. These cystic myomata may reach an immense size and 
fill the abdominal cavity. The diagnosis, during life, between them 
and ovarian cysts is often very difficult, and they have frequently 
been the subjects of fatal operations. The cystic may be lined witii 
ciliated epithelium. 1 

In the cervix uteri myomata are rare. They may grow as polypi 
beneath the mucous coat, or produce enlargement of the anterior or 
posterior lips, or may grow outward into the abdominal cavity. 

Combinations of myoma and sarcoma sometimes occur— myo- 
sarcoma. 

Sarcomata may occur as primary tumors in the mucous mem- 
brane of the uterus, either in the form of a diffuse infiltration or as 
a circumscribed nodular or polypoid mass. They frequently involve 
the muscular wall, are liable to haemorrhage and gangrene, and, 
particularly in the "diffuse form, are liable to recur after removal. 
They may consist largely of spindle or spheroidal cells, or both. It is 
said that sarcoma of the uterus is more liable to occur at an advanced 
age than at an early period, as is the rule with sarcomata of other 
organs. Giant-celled sarcomata have been described. 

Consult monograph by Brens, "Ueber wahre Epithel. fuhrende Cystenbil- 
dung d. Uterus-Myomen, " Leipzig, 1894. 



THE ORGANS OF GENERATION. 



713 



Angioma. — Cavernous angiomata of the wall of the uterus have 
been described. 

Adenoma. — Between a simple adenomatous hyperplasia of the 
mucous membrane of the uterus, on the one hand (see Figs. 332 and 
333), and carcinoma on the other, there is no absolutely sharp mor- 
phological distinction. But there is a considerable group of growths, 
to which the name adenoma is properly applied, which lie on the 
border zone between the distinctly benign and the definitely malig- 
nant new epithelial tissue growths. 

Many epithelial cell growths of the uterus, while adenomatous in 
structure, are so distinctly malignant, and are so liable to develop that 
structural lawlessness characteristic of carcinoma, that it has seemed 




Fig. 336.— Adenoma op the Uterus. 
Showing papillary outgrowths and commencing infiltration of the submucous tissue. 



wise to many observers to avoid the name adenoma altogether and 
class all the epithelial tumors of the uterus among the carcinomata. 
Others, recognizing the benign character of many of the epithelial 
tumors of the uterus, have adopted a sharp distinction between benign 
and malignant adenoma. 

It seems to the writer wise to preserve here, as elsewhere in the 
body, the morphological distinction between adenoma and carcinoma. 
But in doing this it should always be borne in mind that the adeno- 
mata of the uterus, as those of the gastro-intestinal canal, may not 
only be extremely malignant as adenomata, but that the more benign 
forms are extremely prone to develop, both in structure and malig- 
nancy, into carcinomata. In fact, in many cases we can only express 



714 



THE ORGANS OF GENERATION. 



the peculiarities of structure in these tumors by calling them adeno- 
carcinoma. 

The adenomata of the uterus may begin in a simple hyperplasia 
of the mucous membrane, in which glandular development is pre- 
ponderant. This new glandular growth is most common in the 
form of irregular, often dilated follicular structure with a well- 
marked lumen lined with cylindrical or cuboidal cells. The new 
growth may project from the inner surface of the uterus in the form 
of papillary masses, or it may infitrate the submucous tissues. Or 
growth in both directions may occur at once. (See Figs. 336 and 337.) 

The topographical features and clinical stories of many adeno- 



'^rr^ 







Fig. 337.— Adenoma of the Uterus. 
Small portion of specimen shown in Fig. 272, more highly magnified. 



mata of the uterus are identical with those of the infiltrating and 
ulcerating carcinomata. 

Carcinoma. — The carcinomata of the uterus commence most fre- 
quently in the cervix and portio vaginalis, and the most common 
form is the epithelioma. The growth of epitheliomata of the cervix 
uteri proceeds under three tolerably distinct forms, which, however, 
frequently merge into one another. 

1. The Flat, Ulcerating Epithelioma. — This form of cancer 
commences as a somewhat elevated, flat induration of the superficial 



THE ORGANS OF GENERATION. 



715 



layers of the cervix, sometimes circumscribed, sometimes diffuse. 
This induration is due to the growth of plugs and irregular masses 
of epithelial cells into the underlying tissue. Ulceration usually 
commences early and may proceed slowly or rapidly. The edges of 
the ulcer are irregular, indurated, and somewhat elevated. The 
ulceration of the new-formed cancerous tissue at the edges is usually 
progressive, so that the vaginal portion of the cervix, the cervical 
canal, the vagina, and even the^ bladder and rectum may be in- 
volved. More or less extensive haemorrhages and necrosis of the 
base of the ulcer are liable to occur. The entire cervix may be de- 
stroyed. 




Fig. 338— Carcinoma of the Cervix Uteri (Ulcerating). 

2. In another class of cases the carcinomatous growth develops 
under the form of papillary or fungous excrescences, which may 
form larger or smaller masses composed of epitheliomatous tissue. 
Hand-in-hand with this projecting growth there may occur an epi- 
thelial infiltration of the underlying tissue of the cervix. These 
growths are often quite vascular and may give rise to severe haemor- 
rhages. They may ulcerate and thus produce great destruction of 
tissue. 



716 



THE ORGANS OF GENERATION. 



3. In still another class of cases there is a more or less deep infil- 
tration of the submucous tissue, either diffuse or in circumscribed 
nodules, with epithelial cell masses. We find at first, in the vaginal 
portion of the cervix, in the submucous connective tissue, either 
nodules or a general infiltration of a whitish new growth. The cer- 
vix then appears large and hard. Very soon the mucous membrane 
over the new growth degenerates arid falls off; the superficial lay- 
ers of the new growth undergo the same changes. After this the 














Fig. 339.— Carcinoma CEpithelioma) of the Uterus. 
Showing ramifying epithelial cell masses. 



formation of the new growth and its ulceration go on simultane- 
ously, producing first an infiltration and then destruction of the cer- 
vix, and often of a part of the body of the uterus. The growth fre- 
quently extends to the vagina, the bladder, and the rectum with the 
same destructive character, so that we often find the cervix and 
upper part of the vagina destroyed, and in their place a large cavity 



THE ORGANS OF GENERATION. 717 

with ragged, gangrenous, cancerous walls (Fig. 338). Less fre- 
quently the pelvic bones are invaded in the same way. Not infre- 
quently the ureters are surrounded and compressed by the new 
growth, so that they become dilated. The dilatation may extend to 
the pelves and calyces of the kidneys. The new growth may begin 
in the cervix and extend uniformly over the internal surface of the 
cervix and of the body of the uterus. The entire uterus is converted 
into a large sac, of which the walls are infiltrated with the new 
growth, while the internal surface is ulcerating and gangrenous. In 
some cases there is a considerable formation of new, dense connec- 
tive tissue, so that the growth has a scirrhous form. 

In rare cases the growth begins in the upper part of the cervix 
or in the body of the uterus, while the lower part of the cervix is not 
involved. In all of these cases the epithelial cells of the new growth 
follow more or less closely the type of the epithelial cells of the part 
from which they spring (Fig. 339). 

In still another class of cases, in which the new growth may be 
in the form of nodules, or diffuse infiltrations, or polypoid masses, or 
may present more or less extensive alterations, the cells are irregu- 
lar, polyhedral in shape, the tumor belonging to the class of glan- 
dular or medullary carcinomata. These also usually commence in 
the cervix, and, according to the views of many writers, probably 
in the mucous glands. 

In rare cases the entire wall of the uterus is infiltrated with the 
new growth and the organ is much enlarged. Colloid carcinoma 
sometimes occurs, but is rare. 

While we may for convenience recognize the above types of car- 
cinoma of the uterus, it should be borne in mind, as above stated, 
that they are not apt to be perfectly distinct, and some of them may 
merge into one another or exist simultaneously. Exudative inflam- 
mation is of frequent occurrence in these as in other tumors of the 
uterus. 

As a result of the ulceration of these various forms of carcinoma 
Tecto-vaginal fistulae may be formed ; the lumbar lymph nodes may 
be involved, and metastases in distant organs are occasionally 
though not frequently formed. Frequent and profuse haemorrhages, 
gangrenous destruction of tissue, the absorption of deleterious mate- 
rials, etc., are apt to lead to the development of a more or less pro- 
found anaemia and cachexia. 

Decicluoma Malignum. — Under various names several curious 
tumors of the uterus have been described which resemble each other, 
l>ut which differ in structures from any of those in the^ usual lists. 
They are, however, most closely allied to the sarcomata. They all 
occur in the uterus after pregnancy, and all appear to be derived from 
remains of the decidua or its associated structures (Fig. 340). They 
£7 



718 THE ORGANS OF GENERATION. 

frequently give rise to hsemorrhages and are apt to form metastases, 
especially in the vagina and lungs. 

The structure of these tumors varies considerably. The most 
typical forms consist of irregular clusters of trabecula of large irreg- 
ular-shaped cells with prominent nuclei or of masses of protoplasm. 
These cells and cell masses often enclose blood spaces. There is little 
or no stroma. 

On the other hand, some of the tumors in which the connective 
tissue elements more largely share are appropriately called Sarcoma 
deciduo- cellular e. 

Whether these tumors are derived from the foetal or from the 



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Fig. 340.— Fragment of Decidua in Curettings prom the Uterus. 

maternal tissues is not in all cases clear ; perhaps only one or both 
may in the different cases be concerned in the growth. 1 



PARASITES AND CYSTS. 

Various forms of bacteria are of frequent occurrence in the cavity 
of the uterus when the organ is diseased. The presence of some is 
significant, and of others not. Echinococcus has been found in the 
body and neck of the uterus, and may rupture into the peritoneal 
cavity or into the vagina. 

Cysts. — Aside from the cysts which develop in tumors of the 
uterus, in the cervix uteri the mucous follicles are frequently so 
dilated as to form cysts filled with a gelatinous material and more or 
less epithelium. These cysts may be large or small, and are fre- 
quently called ovula Nabothi. Sometimes there is an inflammatory 
growth of new connective tissue about these cysts. In other cases 

1 For a careful description and consideration of these tumors consult the article 
by Williams in the Johns Hopkins Hospital Reports, vol. iv., No. 9, 1895. 



THE ORGANS OF GENERATION. 719 

the cysts may project from the mucous membrane in the form of 
polypi. Similar changes are infrequently found in the body of the 
uterus from the dilatation of occluded uterine glands. Dermoid 
cysts are rarely found in the walls of the uterus. 

THE OY ARIES. 
MALFORMATIONS. 

One or both ovaries may be absent, the other organs of generation 
being also absent or undeveloped. Or the ovaries may be only par- 
tially developed. Absence or arrest of development of one ovary is 
sometimes met with in otherwise well-formed individuals. It is 
sometimes accompanied by a low position of the kidney on the same 
side. The ovaries may pass into the inguinal canal or into the labia 
majora, and remain fixed there through life. Less frequently they 
are found in the crural canal or the foramen ovale. 

CHANGES IN SIZE. 

The ovaries may become larger than normal by chronic inflam- 
mation, by the formation of cysts and tumors. They may become 
atrophied in old age, the Graafian follicles disappearing and the 
organ shrivelling into a small, irregular, fibrous body. Atrophy 
may be produced by ascites, by chronic inflammation, or from un- 
known causes. As the result of the maturing and rupture of the 
Graafian follicles, with and without pregnancy, the surface of the 
ovary, which before puberty is smooth, may become roughened by 
irregular cicatricial depressions. 

CHANGES IN POSITION. 

In adult life the ovaries may pass as hernise into the inguinal or 
•crural canal, the foramen ovale, or the umbilicus. 

The position of the ovaries in the abdomen may be changed by 
the pressure of tumors, the traction of false membranes, etc. It may 
occur in enlarged ovaries or in those of normal size, and by the com- 
pression of the veins may lead to congestion and chronic inflammation 
of the organ. 

HYPEREMIA AND HEMORRHAGE. 

Aside from the normal hypersemia of the ovaries during menstru- 
ation, the vessels may be congested in inflammation, in displace- 
ments with interference with the venous circulation, in certain 
diseases of the heart, etc. , and may then be followed by chronic 
inflammation. 

The menstrual periods are accompanied by the effusion of blood 



720 THE ORGANS OF GENERATION. 

into a Graafian follicle. Normally the amount of blood is small r 
becomes solid, is decolorized and then gradually absorbed. Some- 
times the effusion of blood is much greater ; the follicle filled with 
blood is as large as a pigeon's egg. The blood may remain in the 
follicle and be absorbed, and replaced by a serous fluid, or it may 
rupture it and escape into the peritoneal cavity. Death may ensue 
from the haemorrhage, or the blood may collect in Douglas' cul-de-sac 
and be enclosed in false membranes. Haemorrhages also occur in 
follicles which have become cystic. Interstitial haemorrhage in the 
ovary sometimes occurs without known cause. 

INFLAMMATION (OOPHORITIS). 

Acute Inflammation of the ovaries occurs most frequently in the 
puerperal condition, either as part of a general peritonitis or as a 
primary affection. 

With puerperal peritonitis both ovaries are usually inflamed; 
they are swollen, congested, soft, infiltrated with serum or pus, or 
gangrenous. The inflammation may attack principally the capsule, 
the stroma, or the follicles. Inflammation of the capsule results in 
adhesions and collections of pus, shut in by false membranes ; of the 
stroma, in abscesses and fibrous induration ; of the follicles, in their 
dilatation with purulent serum. If the inflammation of the ovary is 
the primary lesion it is usually confined to one organ. The stroma 
of the ovary is infiltrated with serum and pus, and may contain ab- 
scesses of large size. In other cases the ovary itself is but little 
changed, but is surrounded by a mass of fibrinous and purulent exu- 
dation. Such idiopathic forms of inflammation may terminate in 
recovery ; or the abscesses may perforate into the rectum and va- 
gina ; or the ovary is left indurated and bound down by adhesions ; 
or the patient dies from the violence of the disease. 

Acute inflammation of the ovaries unconnected with the puerperal 
condition is not common, but it may occur in connection with acute 
or chronic peritonitis or perimetritis. It is usually confined to one 
ovary. Either the follicles, stroma, or capsule, or all together, may 
be involved. The inflamed follicles are enlarged, their walls thick- 
ened ; they may contain bloody or purulent fluid. The stroma be- 
comes infiltrated with serum or pus, and later we may find abscesses 
or fibrous induration of the organ. The inflammation of the capsule 
may lead to the formation of membranous adhesions between the 
ovary, Fallopian tube, and surrounding parts. 

Chronic Interstitial Oophoritis is not infrequently preceded by 
an acute inflammation, or it may gradually develop as an indepen- 
dent condition, often determined by some mechanical interference 
with the blood current. The organ may be increased in size, owing 



THE ORGANS OF GENERATION. 



721 



to the formation of loose cellular or of dense, firm, new connective 
tissue. Under these conditions the blood vessels, especially the 
veins, may be widely dilated, and cysts in varying number and size 
maybe present (Fig. 341). Sometimes the new-formed dense con- 
nective tissue may be largely limited to the surface of the organ, so 
that the albuginea may become so dense and thick that the functions 
of the organ must, as it would seem, be permanently interfered with. 
Under these conditions the surface of the ovary may be smooth or 
rough. 

On the other hand, the organ may be smaller than normal as the 
result of the formation of dense new interstitial connective tissue, and 
its surface greatly roughened and distorted. Sometimes the forma- 




^^ : y^>_^^^ 



Fig. 341.— Chronic Oophoritis with dilated Blood Vessels and Cysts. 
a, dense connective-tissue stroma; 6, dilated veins; c, cysts; <3, cyst with granular contents; 
e, cortical zone o£ immature Graafian follicles. 



tion of new dense tissue may be largely confined to the walls of the 
arteries, which become prominent and tortuous. Obliterating en- 
darteritis is not infrequently present. The atrophied ovary may be 
largely made up of thick- walled arteries and fibrous masses which 
are the result of incomplete resolution of the corpora lutea (Fig. 
342). 

Sometimes a more or less extensive hyperplasia of cells in the 
corpus luteum leads to the development of larger or smaller new- 
formed, convoluted, nodular masses in the ovary, which are sometimes 
regarded as tumors. These structures may, according to Freeborn, 
soften at the centre and thus give rise to a special form of small 



722 



THE ORGANS OF GENERATION. 



ovarian cyst. Certain sarcomata of the ovary appear to originate 
in such an hyperplasia (see Fig. 343). 

Tuberculous Inflammation of the ovaries is rare, and may ac- 
company tubercular inflammation of other organs, particularly the 
peritoneum and Fallopian tubes. It usually results in the production 
of cheesy nodules of considerable size. 

Syphilitic Inflammation in the form of gummatais uncommon. 

TUMORS. 

Fibromata. — These tumors are not very common nor usually of 
great importance. They may be very small or of great size. They 
are usually dense in texture, and in a considerable number of cases 
seem to originate in the tissue formed in the closure of the ruptured 

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Fig. 342.— Chronic Oophoritis with Atrophy. 
From a case of valvular disease of the heart with chronic metritis and endometritis, a, thick- 
ened and dense interstitial tissue; b, old corpora lutea; c, arteries with greatly thickened walls; 
d, dilated veins. 

Graafian follicle. They may contain cysts or be accompanied by 
cysts of the surrounding stroma. Papillary fibromata of the surface 
of the ovary are sometimes seen, and the growth may be transplanted 
from this situation to the general peritoneal surfaces (Fig. 344). 

Leiomyomata containing more or less fibrous tissue are of occa- 
sional occurrence. 

Sarcoma of the ovaries is not common. It is usually primary, 
but may be metastatic. It is usually of the spindle-celled variety, 
but may contain areas of spheroidal-celled tissue or more or less 
fibrous tissue. The tumors may be hard or soft, and are apt to in- 
volve both ovaries. Endotheliomata may be found in the ovaries. 

Chondroma of the ovaries is described, but is rare; cartilage not 
infrequently occurs, however, in dermoid cysts. 






THE ORGANS OF GENERATION. 



723 



Carcinoma, usually of the glandular variety, may occur as a 
primary tumor of the ovary. It may be due to a continuous infec- 
tion from neighboring organs, or more rarely it is of metastatic ori- 
gin. Although the glandular medullary carcinomata are the most 
common, scirrhous, melanotic, and colloid cancer sometimes occur. 
Some forms of carcinoma stand in very close relation with certain of 
the cystic adenomata (see below). 

Adenomata (Cystic Adenomata ; Compound Ovarian Cysts). — 
These growths, which may occur in one or both ovaries, form one of 
the most common and important classes of ovarian tumors. Some 
of their most noteworthy and important features depend upon their 




1 <, / > : V» -V- ■- :. ( -'- £, -: v - % 

Fig. 343.— Commencement oe Sarcomatous Growth in the Ovary. 
From hyperplastic cells of corpus luteum. Specimen prepared by Dr. G. C. Freeborn. 

tendency to the formation of cysts. It should be remembered, how- 
ever, that the primary lesion is a true new formation of glandular 
tissue, and not, as in the case of most cysts, a transformation, by re- 
tention or otherwise, of pre-existing structures. 

The growth primarily consists of a fibrous stroma, in which are 
tubular follicles lined with cylindrical epithelium. Or, in some cases, 
it consists of papillary outgrowths from a fibrous stroma, which are 
covered with cylindrical epithelium. 

Glandular Cyst-Adenoma. — There is, as above stated, a marked 
tendency, particularly in the glandular form of adenoma, to a dilata- 



724 



THE ORGANS OF GENERATION. 



tion of the follicles by a semi-fluid material, and the formation of 
o ysts. There may be a number of follicles equally dilated, so as to 
form a number of cysts of moderate size ; or only a few follicles are 
enormously dilated to form a large multilocular cyst with but few 
compartments. The walls of the cysts may fuse together and be ab- 
sorbed, so as to form one large cyst divided by incomplete septa — uni- 
locular cysts. The stroma in which the follicles and cysts are em- 
bedded may be largely developed or very scanty. 







Fig. 344.— Papilloma op Peritoneum. 
Transplanted from a similar growth on the surface of the ovary. 

The walls of the larger cysts are composed of fibrous tissue which 
is dense in the outer layers, more cellular in the inner, upon which 
the epithelium is placed. They may be thin and membranous, or we 
find developed on their internal surfaces an intracystic growth com- 
posed of a fibrous stroma and tubular follicles. These secondary 
follicles may also be filled with fluid and form larger and smaller 
cysts. The intracystic growths may be so large as to fill up the 
original cysts. Sometimes the intracystic growth presents very little 
dilatation of its follicles, so that the entire tumor has more the cha- 
racter of a solid growth than of a cyst. 



THE ORGANS OF GENERATION. 



725 



The cylindrical epithelium lining the cysts usually forms a single 
layer (Fig. 345), but, owing to the accumulation of fluid, the cells 
may become flattened and atrophied, or they may be fatty or desqua- 
mated. The contents of the cysts differ considerably in different 
cases, and even in different cysts in the same case. They may be 
tough and ropy, or gelatinous or serous ; transparent and colorless, 
or yellow or reddish, or reddish-brown ; or they may be turbid and 
colorless, or variously colored — red, brown, or chocolate. 

Chemically the cyst contents, when thick and ropy, contain mucin 
or paralbumin, and perhaps other less well-known compounds belong- 
ing to the same class. It is believed that the peculiar ropy character 
which the fluid often possesses is due to the paralbumin, but the 
chemical nature and relations of this substance are still matters of 






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Fig. 345.— Cystic Adenoma of Ovary. 
Glandular form. 



dispute. It is probable that the contents of these cysts are, so far 
as the mucin and paralbumin are concerned, produced by a meta- 
morphosis of the protoplasm of the lining cells, similar to that by 
which the mucin is produced in the mucous glands and in mucous 
membranes. We frequently find the cylindrical cells presenting the 
form of the so-called "beaker cells," and in some cases the mucous 
contents of the cysts are seen to be continuous with the similar con- 
tents of the beaker cells. It is probable that much of the fluid con- 
tents of the cysts comes from simple transudation. 

Microscopically the contents of these cysts present also considerable 

variation. We may find almost no structural elements ; or there 

may be red blood cells in variable quantity, and pus cells in various 

stages of granular or fatty degeneration or of disintegration, so that 

58 



726 



THE ORGANS OF GENERATION. 



variously shaped fragments of the cells appear. Then we may find 
cylindrical, or flattened, or polyhedral cells, either well preserved, 
swollen, or in a state of fatty degeneration (Fig. 346), or we may 
find fragments of these cells. It is these various forms of cells, often 
more or less swollen and in a condition of more or less well-marked 




Fia. 346.— Cells from Contents of an Ovarian Cyst in a Condition of Fatty Degeneration. 

granular and fatty degeneration, which have been considered cha- 
racteristic of the ovarian cysts and are sometimes called Drysdale's 
corpuscles. While, however, they are of frequent occurrence under 
these conditions, they are by no means pathognomonic, since we find 
them in the contents of various kinds of cysts and cavities where the 
cells are undergoing degeneration. In addition to the above struc- 




Fig. 347.— Cystic Adenoma of Ovary (Papillary form). 

tural elements we may find free fat droplets, cholesterin crystals, 
pigment granules, and more or less granular detritus. The material 
filling these cysts is sometimes called colloid, and the cysts are fre- 
quently called colloid cysts ; but we believe that the above view of 
their nature is the correct one. 

Numerous secondary changes are liable to occur in these cysts. 



THE ORGANS OF GENERATION. 



727 



The cells may become fatty and peel off, so that we may find in some 
parts only a connective-tissue wall. The walls may atrophy, may 
become infiltrated with salts of lime, or contain concentrically lamel- 
lated lime concretions. Inflammatory changes may occur in them. 
There may be a suppurative inflammation of the walls leading to 
the formation of abscesses, or pus may be mingled with the cyst 
contents ; the epithelium may be exfoliated and granulation tissue 
may form in the walls. Chronic inflammation may lead to consider- 
able thickening of the walls and to adhesions with neighboring parts. 
Haemorrhages, sometimes very extensive, may occur in inflammation, 
or as the result of other disturbances of the circulation, so that some 
oi the cysts may be filled with blood. Inflammatory softening, gan- 
grene, etc., of the walls may lead to perforation, so that the contents 




Pig. 348.— Multiple Papillary Cysts of the Omentum, secondary to a similar Growth in the 

Ovary. 
The papillary outgrowths are themselves becoming: softened at their centres, forming acces- 
sory cysts. Drawn from specimen loaned by Dr. G. C Freeborn. 

of the cysts may be discharged into the peritoneal cavity, or, in 
virtue of adhesions, into the bladder, vagina, or rectum. Carcinoma 
may be developed from the epithelium of the cysts. Since these 
cysts sometimes reach a very large size, they may produce the greatest 
variety of disturbances in the abdominal cavity, which need not be 
enumerated here. 

They probably originate in the glandular epithelium of the ovary 
either before or after the formation of the Graafian follicles. 1 



1 For more extended descriptions of the cyst- adenomata of the ovaries see Wal- 
deyer, "Die epithelialen Eierstocksgeschwtilste," Archiv fiir Gynakologie, Bd. i., 
Heft 2, pp. 252-316, 1870. Also Elebs, " Handbuch der pathologischen Anatomie," 
vierte Lieferung, p. 796, 1873. Pozzi, "Treatise on Gynaecology," edited by Brooks 
H. Wells, M.D., 1892, 



728 



THE ORGANS OF GENERATION. 



Papillary Cyst-Adenoma. — This form of cyst-adenoma was 
formerly regarded as but a variety of the form above described — a 
variety characterized by papillary outgrowths in cauliflower-like 
tufts from the walls of the cysts, which often in large degree fill the 
cyst spaces (Fig. 347). There appears, however, to be sufficient evi- 
dence, both anatomical and clinical, to justify the separation of the 
papillary from the glandular form of cyst-adenoma. 

The papillary cyst-adenomata are not, as a rule, as large as the 
glandular form. The cysts are fewer and they do not contain colloid 
material. The papillary outgrowths often break through the cyst 




Fig. 349. 



-Adeno-Sarcoma of the Ovary (Endothelioma 1 ;'). 
Specimen loaned by Dr. G. C. Freeborn. 



walls, and may be transplanted to the peritoneal or other surfaces in 
the form of multiple cystic or papillary tumors (Fig. 348). The 
papillae and cyst walls may be lined by cylindrical and often by cil- 
iated epithelium. They may develop from the follicular or germinal 
epithelium, and probably, according to Williams, sometimes from 
the tubular epithelium. 1 

Cyst-adenomata of the ovary may, through an unusual prolifera- 



1 Williams, Johns Hopkins Hospital Reports, 
Amer. Jour, of Obstetrics, June, 1895, p. 846. 



vol. iii., 1893; also Freeborn. 



THE ORGANS OF GENERATION. 729 

tion of the epithelial cells, form such dense, closely packed cellular 
masses that the type of structure seems changed. Such a change is 
shown in Fig. 349, in which, in addition to the excessive production 
of epithelium, the stroma is sarcomatous. 

Follicular Cysts of the Ovary. — The Graafian follicles may be 
dilated so as to form cysts. This may occur in one or both ovaries, 
and the cysts may be small or large, single or multiple. They are 
usually found after middle life, but may occur during youth, child- 
hood, or even in the foetus. The follicles dilate from the accumula- 
tion of fluid within them ; the ovum is destroyed, the epithelium 
flattened. The contents are usually serous and colorless, but may be 
viscid, turbid, purulent, or variously colored, red, yellow, or brown. 
The ovary may be crowded with numerous cysts of moderate size, 
whose adjacent walls may coalesce and atrophy, forming communi- 
cations between them. 

A variety of this form of cyst is formed by the dilatation, either 
with or without the hyperplasia above described, of a corpus luteum. 
Such cysts may communicate with a Fallopian tube. 

Dermoid Cysts. — These cysts may be uni- or multilocular, are 
xisually of moderate size, but sometimes become as large as a man's 
head or larger. Their fibrous walls may be thick or thin, and por- 
tions of the internal surface may present more or less completely de- 
veloped cuticular structures, such as corium, papilla, epidermis, hairs 
and hair follicles, sebaceous glands, etc. The cavity may contain a 
thick, whitish, greasy material composed of flattened epithelium, fat, 
or cholesterin crystals. Or the cavity or walls may contain masse? 
of irregularly formed hair, teeth, bone, cartilage, striated muscle, 
and nerve fibres and cells. Such growths, which are doubtless of 
embryonal origin, may exist for many years without causing incon- 
venience ; but inflammatory changes may occur in them, leading to 
adhesions and perforations into adjacent organs. They may form 
the nidus for the development of carcinoma, or they may calcify. 

In addition to the above-described adenoid, dermoid, and simple 
follicular cysts, there are a number of composite forms of not infre- 
quent occurrence. Thus, in connection with dermoid cysts or sepa- 
rately, we find larger and smaller cysts lined with ciliated epithe- 
lium. Then there are several cases described of cysts which partake 
of the characters of both adenoid and dermoid cysts. Such cysts 
may be multilocular and be lined with flattened, cylindrical, or 
ciliated epithelium, and may contain epidermal cells, cholesterin or 
mucin, etc. 

Small cysts, sometimes pediculated, sometimes not, of doubtful 
origin and usually of no special significance, are frequently found 
growing from the broad ligament near the ovary. The walls are 






730 



ORGANS OF GENERATION. 



■usually very thin, lined with flattened epithelial cells, and the con- 
tents serous. Solid teratomata are of occasional occurrence in the 
ovary . J 

Cysts of the Parovarium, lying between the peritoneal layers of 
the broad ligament, are usually small, but may be as large as a man's 
head. They are usually lined with ciliated epithelium, but some- 
times with flattened non-ciliated cells. The contents may be serous, 
or may be thick and contain mucin and paralbumin. 

THE FALLOPIAN TUBES. 

MALFORMATIONS. 

Absence of both tubes occurs with absence of the uterus. One 
tube may be absent, with arrested development of the corresponding 




Fig. 350.— Hydro salpinx. 

side of the uterus. Both tubes may be imperfectly developed ; either 
of their ends may be closed ; they may be inserted into the uterus at 
an abnormal place ; they may terminate in two or three abdominal 
ostia. 

CHANGES IN POSITION AND SIZE. 

The Fallopian tubes may participate in the various malpositions 
of the uterus and ovaries ; but they are most frequently displaced by* 
the contraction of adhesions formed in perimetritic and periovarial 
inflammations. 

The lumen of the tube may be partially or completely closed as 
the result of inflammation of the mucous membrane ; of peritonitis 
about the fimbriated extremity ; of tumors or inflammation of the 

1 Consult Wilms, Ziegler's Beitr. z. path. Anal, Bd. xix., p. 367, 1896. 



THE ORGANS OF GENERATION. 731 

uterus ; or by pressure from without, or by adhesions, tumors, etc. 
It may become stopped by plugs of mucus or pus. 

Dilatation of the tubes may be produced by an accumulation of 
catarrhal or other exudation, when there is partial or complete ste- 
nosis at some portion of the tube. The dilatation may be moderate, 
converting the tube into a tortuous, sacculated canal containing 
mucous or serous fluid ; or, more rarely, large cysts may form con- 
taining several pounds of serous fluid — hydrosalpinx (Fig. 350). 
As the fluid collects the epithelium may become flattened or fatty 
or may desquamate. As a result of an inflammation in the walls of 
the dilated tube, the contents may be mixed with pus or blood. Rup- 
ture of a dilated tube sometimes occurs ; or severe and even fatal 
haemorrhage may take place into its cavity. Papillary growths 
are sometimes found springing from the inner wall of the cysts. 

HEMORRHAGE. 

Haemorrhage into the tube may occur in puerperal women with 
retroversion of the uterus, with abortions ; haematometra and tubal 
pregnancy ; in acute infectious diseases. The blood may undergo 
degenerative changes and be largely absorbed, or it may escape into 
the peritoneal cavity and cause peritonitis. 

INFLAMMATION (SALPINGITIS). 

Catarrhal Inflammation of the mucous membrane of the Fallo- 
pian tubes commonly occurs in connection with endometritis, fre- 
quently in the puerperal condition. In the acute stage the mucous 
membrane is hyperaemic and swollen, and covered with a muco- 
purulent exudation. The inflammation may subside, leaving no 
lesions, but it more frequently becomes chronic, and may then result 
in peritoneal adhesions, thickening of the walls, obliteration of the 
tubes, dilatation, etc. 

Suppurative Salpingitis. — This inflammation of the mucous 
membrane may assume a suppurative character, particularly in con- 
nection with puerperal metritis and peritonitis, but sometimes as a 
result of gonorrhoeal inflammation. 

Under these conditions the wall of the tube may be involved and 
pus may exude from the abdominal ends. It is difficult, in many 
cases of suppurative salpingitis associated with peritonitis, to say 
which is the primary lesion. 

In some cases there is a considerable collection of pus in the tubes, 
causing dilatation— pyo-salpinx. These collections may rupture 
into the peritoneal cavity, or the pus may escape into a cavity shut 
in by adhesions, or may perforate into the intestine or bladder. Or 
it may dry and finally become calcified. 



732 THE ORGANS OF GENERATION. 

Suppurative salpingitis is believed to be most commonly caused 
by the gonococcus or the pyogenic bacteria. 

Tuberculous Inflammation. — This form of inflammation in the 
tubes is most frequently seen in its later stages, when the mucous 
membrane is partially or entirely converted into a thick, cheesy, 
often ulcerating layer. The lumen of the tubes may be dilated, the 
walls thickened from chronic inflammation. This lesion may occur 
by itself, or may be associated with tubercular inflammation of the 
lungs, or of the other genito-urinary organs, or of the peritoneum. 
The lesion usually commences at the • abdominal ends of the tubes, 
and both tubes are apt to be involved. 

Syphilitic Inflammation, in the form of a diffuse thickening of 
the wall by gummatous tissue, has been described. 

TUMORS. 

Small fibromata and fibro-myomata sometimes occur in the 
wall of the tubes or in the fimbriae. Small lipomata have been seen 
between the folds of the broad ligament in close connection with the 
tubes. 

Carcinoma of the tubes is usually, if not always, secondary to 
carcinoma of the uterus or the ovaries. 

Cysts, usually of small size, sometimes pediculated and with thin 
walls, are frequently seen in the peritoneal covering of the tubes or 
in the fimbriae. They are believed to be of embryonal origin. 

Dilatation of the tubes, as above described, may convert them 
into cyst-like structures. 

EXTRA-UTERINE PREGNANCY. 

Tubal Pregnancy. — The impregnated ovum is in some way hin- 
dered from passing into the uterus, becomes fixed in the tube, and 
is there developed. The villi of the chorion grow into the mucous 
membrane of the tube, forming an incomplete placenta. Rare cases 
are recorded in which the placenta was situated in the uterus while 
the foetus was developed in the tube. The embryo and its mem- 
branes are developed until they reach such a size that the tube sur- 
rounding them ruptures. This may occur in the first month or not 
until much later. In rare cases, when the wall of the tube was ex- 
tensively involved in the formation of the placenta, the development 
has gone on until term. The ovum may remain in the tube after the 
rupture ; or may escape into the peritoneal cavity, still enveloped in 
its membranes ; or the membranes may be ruptured and left in the 
tube. The rupture is generally attended with fatal haemorrhage. In 
some cases death is caused by the rupture of a dilated vein while the 



i. 



THE ORGANS OF GENERATION. 733 

tube is still intact. Haemorrhage into the sac may occur before its 
rupture. 

In rare cases death does not take place and the foetus is shut in 
by adhesions and false membranes. The embryo soon dies. In fa- 
vorable cases there is a slow absorption of the soft parts of the foe- 
tus, the bones are separated and left embedded in a mass of fibrous 
tissue, fat, cholesterin, and pigment ; or the foetus retains its shape 
and becomes mummified, and may then be encrusted with the salts 
of lime (Hthopedion). 

In unfavorable cases degeneration and gangrene of the foetus take 
place rapidly, with inflammation and suppuration of the surround- 
ing tissues. There may be perforation and escape of the broken- 
down foetus through the rectum, vagina, bladder, or abdominal wall. 
The patient may die from peritonitis or exhaustion, or may recover 
after the escape of the foetus. 

In some cases the foetus may escape through a rupture of the tube 
into the space between the folds of the broad ligament. 

Tubo- abdominal Pregnancy is produced by the development of 
the ovum in the fimbriated extremity of the Fallopian tube. Adhe- 
sions are formed, so that the foetus is partly in the end of the tube and 
partly in the abdomen. 

Interstitial Pregnancy. — The ovum in these cases is arrested 
and developed in the portion of the tube which passes through the 
wall of the uterus. 

Abdominal Pregnancy. — The ovum, after escaping from the 
ovary, does not enter the Fallopian tube, but becomes fixed to the 
peritoneum, usually at some part near the ovary. It is surrounded 
by thickened peritoneum and develops in that position. 

Ovarian Pregnancy. — The existence of this form of pregnancy is 
doubtful and difficult to prove, but there are some cases in which it 
seems probable that the ovum develops in its Graafian follicle. The 
placenta may be attached to the tube or to the abdominal wall. 

In all forms of extra-uterine pregnancy the uterus becomes en- 
larged and a sort of decidua is formed on its internal surface. 

LESIONS OF THE PLACENTA. 1 

Aside from the variations from the normal in size, shape, and po- 
sition, for a description of which we refer to the works on obstet- 
rics, we may briefly mention here some of the more important struc- 
tural changes which the placenta may undergo. 

Hcemorrhage. — This may occur either on the maternal surf ace in 
the decidua ; or between the foetal surface and the membranes ; or in 
the substance of the placenta. The latter form of haemorrhage con- 

1 For structure of placenta consult Eden, Journal of Pathology and Bacteriology, 
vol. iii., p. 449 (bibliography). 






. 



734 THE ORGANS OF GENERATION. 

stitutes the true placental apoplexy. This may occur as the result 
of rupture of a placental sinus. The placental tissue is crowded 
apart, and a blood clot, often infiltrating the parenchyma, is formed. 
This may lead to abortion, or the blood may undergo disintegration 
and absorption and its place be occupied by a cicatrix. The placen- 
tal tissue in its vicinity may undergo fatty degeneration. Under 
other conditions, without evidence of rupture of the vessels, the pla- 
cental tissue may become infiltrated with blood in the form of an in- 
farction. In this, degenerative changes similar to the above may oc- 
cur, leading to fibrous induration of the placenta. 

The so-called "white infarctions " of the placenta appear to be al- 
tered thrombi in the maternal blood spaces. They consist of lamel- 
lated or homogeneous or fibrillar fibrin, and form important larger 
and smaller yellowish-white or reddish, irregular masses, and appear 
to be of pathological significance only when they occur early or are 
of great extent. 

INFLAMMATION (PLACENTITIS). 

Suppurative Inflammation of the placenta, with the formation 
of abscesses, is of rare occurrence as the result of injury. 

Chronic Indurative Inflammation of the placenta may result 
in the formation of circumscribed masses of cellular and loose, or 
dense and cicatricial, connective tissue, or in a diffuse formation of 
connective tissue, which may interfere with the nutrition of the foetus 
and cause abortion. The new-formed connective tissue may undergo 
fatty degeneration or calcification. 

In another class of cases the new connective tissue is formed 
mainly in the walls of the vessels, particularly the arteries. This 
may occur in circumscribed portions of the vessels, leading to nodular 
growths around the arteries, or it may occur extensively along the 
various ramifications of the vessels, converting them into thick 
fibrous cords. The change is primarily in the adventitia, but all the 
coats of the vessel may become involved, leading to more or less 
complete obliteration of the lumen. 

Various proliferative and indurative changes in the placenta may 
occur as the result of syphilitic infection. 

DEGENERATIONS. 

Fatty and amyloid degeneration and calcification of the placental 
tissue are of not infrequent occurrence. 

Cysts of the placenta are of occasional occurrence ; their origin is 
in most cases obscure. 1 

1 See Ahlfeldt, Arch, fur Gynakologie, Bd. ii., p. 397. Fenomenodes, ibid., BcL 
xv., p. 343. Hofmeier, " Die menschliche Placenta," 1890. 



THE ORGANS OF GENERATION. 735 

Fragments of placenta remaining in the uterus after delivery 
may serve as a nidus for a- blood thrombus, or they may undergo 
proliferation, thus forming tumors, deciduomata (see page 718). 

An hypertrophy of the villi of the chorion may give rise to the 
fibrous structures known as fibrous moles. When to the fibrous 
change mucous degeneration is added the so-called hydatid moles 

are formed. 1 

THE MAMMA. 

MALFORMATIONS. 

Absence of both mammae is only found in connection with other 
marked malformations. 

Absence of one mamma has been observed in a few cases, with 
and without defective development of the corresponding half of the 
thorax. 

Absence of one or of both nipples is more common. 

Arrest of development of the mammae is found in connection with 
arrest of development of the organs of generation, and, to a less 
degree, alone. 

Supernumerary mammae and nipples have been observed in a 
number of cases. The glands may all secrete milk during lactation. 

Too early development of the mammae is sometimes found in 

young children in connection with abnormal development of the 

organs of generation. 

HAEMORRHAGE. 

In young women who suffer from amenorrhcea or dysmenorrhea, 
small hsemorrhages sometimes occur in the mammae at the time of 
menstruation. The blood may find its way into the milk ducts and 
exude in small quantities at the nipple. 

Contusions of the breast may produce extravasations of blood in 
the mammary gland or the surrounding connective tissue. This may 
become absorbed, or may remain and be surrounded by fibrous tissue 
or be converted into cysts. 

INFLAMMATION. 

During lactation the nipple is liable to become inflamed in three 
ways, which may occur separately or be combined together. 

1. The epidermis is rubbed off by nursing, the cutis becomes in- 
flamed and converted into granulation tissue ; in this way small or 
large ulcers may be formed. 

2. Fissures are formed at the base of the nipple, which extend 
completely through the skin, and are lined at the bottom with granu- 
lation tissue. 

1 Consult Marchand, Zeits. f. Geburtsh. u. Gynak., Bd. xxxii., p. 405; also 
Fraenlrl, Arch. f. Gynak., Bd. xlix.. 



736 



THE ORGANS OF GENERATION. 



3. There is a diffuse inflammation of the whole nipple, which does 
not, however, go on to suppuration. The nipple is conical, red, 
swollen, and very painful. 

There is a form of eczema-like inflammation of the nipple and 
areola which tends to ulcerate and develop into carcinoma. This is 
known as Paget's disease, and is believed by some observers to be 
associated with coccidia (see page 129). 

Acute Inflammation of the Mamma (Mastitis) occurs most fre- 
quently during lactation ; it also occurs during pregnancy, and 
occasionally in women who are neither pregnant nor nursing. 




Fig. 351.— Suppurative Mastitis occurring in the Non-functionating Gland. 

a, milk duct; 6, interstitial tissue; c, dense collections of pus; d, diffuse infiltration of lobule 
with pus. 



The inflammation may involve the subcutaneous connective tissue, 
the gland itself, or the connective tissue between the gland and the 
wall of the thorax. The inflamed tissues are at first congested, 
swollen, hard, and painful. The inflammation may stop at this point 
and resolution take place, but more frequently it is succeeded by 
suppuration. If the inflammation involves the subcutaneous con- 
nective tissue the abscess may be superficial and soon open through 
the skin. If the gland is involved one lobule after another may 



THE ORGANS OF GENERATION. 



73? 



become inflamed (Fig. 351), so that successive abscesses are formed 
in different parts of the gland. If the connective tissue beneath the 
gland is inflamed a deep abscess of large size may be formed, which 
usually perforates through the skin, but sometimes into the pleural 
cavity. In both these latter forms of abscess there is apt to be ne- 
crosis of large portions of tissue. These abscesses may cicatrize, or 
they may pass into a chronic condition and remain as suppurating, 
fistulous tracts for a long time. Suppurative mastitis is usually due 
to the presence of Streptococcus and Staphylococcus pyogenes. 

In new-born children there is often a painful swelling of the 
breasts, which usually subsides in a few days, but may go on to 
suppuration. 

Epidemic parotitis is sometimes complicated by mastitis. 

Chronic Inflammation of the interstitial connective tissue of the 





M5&8T# 




Fig. 352.— Chronic Inflammation of Mammary Gland. 



mammary gland may result in the formation of dense connective 
tissue (Fig. 352), with or without cystic dilatation of the milk ducts 
and atrophy of the glandular elements. Acute exudative inflamma- 
tion may occur in a gland which is the seat of chronic inflammation, 
and abscesses may be formed. 

Eczema sometimes affects the skin of the nipple. Attention has 
lately been drawn to the relationship between this inflammation and 
carcinoma of the nipple, for the two are frequently associated. It is 
possible that the eczema may lead to the subsequent development of 
the carcinoma. 

Tuberculous Inflammation of the mammary gland and its excre- 
tory ducts is of occasional occurrence. It may manifest itself in the 
form of miliary tubercles, larger and smaller cheesy masses of new- 
formed tissue, or cold abscesses. 



738 



THE ORGANS OF GENERATION. 



Syphilitic ulcers may occur in the nipple either as primary chan- 
cres or as mucous patches. Gummy tumors have been observed in 
the mamma. 

TUMORS. 

There may be a general hypertrophy of one or both breasts. 
This is usually found in young, unmarried women, but sometimes in 




Fig. 353.— Intracanalicular Fibroma op the Mamma, x 170 and reduced. 
Cross-section of a milk duct with polypoid ingrowths. 

advanced life. There is an increase in all the elements of the gland, 
both the glandular and the connective-tissue. 

Cysts of the mamma seem to be for the most part retention cysts, 
formed by the dilatation of the glandular ducts or acini. During 
lactation such retention cysts are sometimes formed, and then con- 
tain milk. They may reach an enormous size. At other times re- 
tention cysts are formed containing serous or viscid, brownish fluid, 



THE ORGANS OF GENERATION. 



39 



which often exudes through the nipple. These cysts may be large or 
small, single or multiple. There is usually at the same time some 
growth and induration of the connective tissue of the gland. In 
some cases there are polypoid outgrowths of connective tissue from 
the wall of the cyst. These cysts are not to be confounded with the 
cysts which are developed with the intracanalicular tumors, of which 
we shall speak below. 

Fibroma. — Circumscribed tumors composed of connective tissue 
are sometimes found in the breast. They are dense and hard, and 
may enclose in them some of the gland ducts and acini. 

Intracanalicular Fibroma. — These tumors are formed by a dif- 







Fig. 354.— Pericanalicular Fibroma of the Mamjia. 



fuse growth of connective tissue, a dilatation of the milk ducts, and 
a growth of polypoid fibrous tumors from the walls of the ducts into 
their cavities. The glandular acini may be atrophied, or enlarged, 
or cystic. A section of such a tumor looks like a solid mass of fibrous 
tissue, divided by clefts and fissures lined with cylindrical or cuboidal 
epithelium (Fig. 353). or containing cysts into which project poly- 
poid fibrous outgrowths. These tumors grow slowly, but if left to 
themselves may reach an enormous size. The skin over them may 
ulcerate and the tumor project through the opening in fungous 
masses. 

Pericanalicular Fibroma. — Sometimes the new connective tissue 
forms a more or less thick cvlindrical investment of the duct with- 



740 THE ORGANS OF GENERATION. 

out growing into its lumen. This formation, which is shown in Fig. 
354, is sometimes called pericanalicular fibroma. 

Myxoma. — This form of tumor may occur as a circumscribed 
growth replacing part of the mamma, or it may be developed in the 
same way as the intracanalicular fibromata. It is not uncommon in 
these intracanalicular tumors to find a combination of fibrous, mu- 
cous, and sarcomatous tissue in the same tumor. 

Chondroma is a very rare form of tumor in the mamma. A few 
cases have been described in which it was combined with carcinoma. 

Adenoma. — Tumors composed of glandular acini, and ducts sur- 
rounded by connective tissue, are of frequent occurrence in the 
mamma (Fig. 145). They are either single or multiple, or sev- 
eral may be developed successively in the same breast. They grow 
at first slowly, afterward more rapidly. Their structure may be 
further complicated by the dilatation of one or more of the ducts 
which compose the tumor into cysts, and the ingrowth of connective 
tissue from the walls of these cysts. 

Sarcoma. — This form of growth may be developed as a circum- 
scribed tumor of small or large size. Its basement substance is that 
of connective or of mucous tissue, and may be scanty or abundant. 
The cells are spheroidal, fusiform, branched, or polygonal. These 
tumors may simply replace the gland ; or glandular acini and ducts 
may be enclosed within them ; or these ducts and acini may be di- 
lated so as to form cysts ; or there may be a new growth of the gland 
tissue so as to form an adeno-sarcoma. 

In other cases the sarcoma takes the intracanalicular form. 
There is a diffuse growth of sarcomatous tissue, a dilatation of milk 
ducts, and an outgrowth of sarcomatous tissue from the walls of the 
dilated ducts into their cavities. These tumors often reach an enor- 
mous size, and there is apt to be ulceration of the skin over them. 

Carcinoma of the mamma is most common in women between 
the ages of thirty-five and fifty-five, but it sometimes occurs in 
women not over twenty years old, and sometimes in old persons. It 
occurs in either breast, in the right rather more frequently than in 
the left, but sometimes in both. The growth begins more frequently 
at the periphery of the gland than at its centre, and more frequently 
in the upper edge of the gland than in any other place. 

The growth most frequently begins as a small, circumscribed 
nodule, which enlarges and involves more and more of the breast ; 
sometimes, however, it is diffuse from the first, and sometimes it be- 
gins in the nipple. 

It may infiltrate the adjacent tissues and the axillary and cervical 
glands, and form metastatic tumors in different parts of the body. 

There are several different anatomical forms of the growth : 






THE ORGANS OF GENERATION. 741 

1. Those in which the epithelial elements preponderate, the soft 
or so-called medullary carcinomata. 

2. Those in which both the connective-tissue stroma and the 
epithelial cells are prominently developed, the cells lying in well- 
defined larger and smaller irregular-shaped spaces, so that the simu- 
lation of gland tissue is tolerably close. These are called carcinoma 
simplex. 

3. The tumors in which the connective- tissue stroma preponder- 
ates, giving the tumor its hard, dense character. This is the carci- 
noma fibrosum, or scirrhous. 

Colloid carcinoma of the mamma is rare. Various secondary 
changes may occur in these tumors, such as have been described in 
the section on Tumors. 

In any of these forms of cancer there may be cystic dilatations of 
the ducts and acini. 

Besides the primary carcinomata of the mamma, secondary car- 
cinomata are met with in rare cases. 



MALE GENERATIVE ORGANS. 
THE PENIS. 

MALFORMATIONS. 

Entire absence of the penis is met with in connection with great 
defects of development of the rest of the body. 

Absence of the penis, with proper development of the other 
organs of generation, is rare. The urethra then usually opens into 
the rectum. 

An abnormally small penis is found, with absence or arrested de- 
velopment of the testicles. 

Absence or a rudimentary form of the prepuce has been observed 
in a number of cases. Congenital phimosis is also not infrequent. 

Hypospadia consists in an arrest of development of the penis 
and scrotum. In its highest degree the penis is one-half to one inch 
long, the glans penis small and resembling a clitoris. On the lower 
side of the penis is a deep cleft lined with mucous membrane. Into 
this cleft the urethra opens at the root of the penis. The scrotum 
remains separated into two halves, resembling labia majora. The 
testes descend into their proper position on each side or remain in 
the abdomen. If the testicles continue to develop normally the in- 
dividual has the appearance and capacities of a man ; if their de- 
velopment is arrested the individual is small and has a womanish ap- 
pearance. 
59 



742 THE ORGANS OF GENERATION. 

In lesser grades of the same malformation the two halves of the 
scrotum are joined and the penis is larger, but a part of the urethra 
remains open as a cleft at any point of the penis. 

Epispadias is an opening of the urethra on the upper side of the 
penis. It presents various grades and forms. 

Hermaphroditism. — This is a union of two sexes in the same 
person, the test of which is the presence of the secreting organs, the 
ovaries and testicles. True hermaphroditism is rare, but it does 
occur, while most of the conditions called hermaphroditism are in 
reality due to varying malformations of the external generative 
organs. 

Pseudo-hermaphroditism. — This malformation consists in an 
abnormal change in the transition from the foetal condition of the 
parts to their fully developed form. In the male, normally, the 
greater part of Miiller's canal disappears and its lower end forms the 
vesicula prostatica. In this malformation Muller's canal is changed, 
as it is in the female, into Fallopian tubes, uterus, and vagina, while 
at the same time the testes, epididymes, vesiculae seminales, and 
spermatic cord are formed as usual. In the lesser degrees of this 
malformation we find, in the place of the vesicula prostatica, a pear- 
shaped sac as large as a pigeon's egg, with muscular walls and an 
epithelial lining. This sac may be incompletely divided into a ute- 
rus and vagina, and it opens into the urethra. In the higher grades 
we find a well-formed vagina and uterus. The uterus may or may 
not have Fallopian tubes. The testicles are usually retained in the 
abdomen or inguinal canals, and are small. The spermatic ducts 
run on the sides of the uterus and open into the urethra or are 
closed. The penis and scrotum appear as in hypospadia, or are well 
formed. The appearance of the individual varies with the develop- 
ment of the testicles. 

True Hermaphroditism may be lateral. In this condition there 
is hypospadia ; a vagina and uterus and a Fallopian tube and ovary 
on one side, and a testicle and spermatic cord on the other. 

In certain cases, which may be called bilateral hermaphrodit- 
ism, there is a testicle on one side and an ovary on the other. l 

Enlargement of the penis is sometimes caused by venous conges- 
tion from heart disease ; by long-continued .masturbation, as a result 
of which the corpus cavernosum may lose its contractility ; and in 
rare cases by hypertrophy of the stroma of the corpus cavernosum. 



1 For a detailed consideration of the malformations of the male and female gene- 
rative organs consult Klebs, " Handbuch der pathologischen Anatomie," and more re- 
cent cases of hermaphroditism by Heppner, Arch. f. Anat. u. Physiol., 1870, and by 
Hofmann, Wien. med. Jahrb., 1877. 



THE ORGANS OF GENERATION. 743 

Injury and Haemorrhage. — Injuries to the penis are liable to 
give rise to severe haemorrhage on account of its peculiar vascu- 
lar character ; suppurative inflammation, gangrene, infiltration with 
urine and its consequences, are also liable to occur. The contractions 
of the cicatricial tissue by which wounds are healed frequently give 
rise to various distortions of the organ and not infrequently prevent 
subsequent erections. 

INFLAMMATION. 

Balanitis, inflammation of the prepuce, is usually produced by 
gonorrhoea or by accumulations of smegma. The skin is red and 
swollen and may ulcerate. Condylomata may be formed, and adhe- 
sions between the prepuce and glans. The glans may ulcerate and 
the prepuce may be much thickened. If the prepuce is long there is 
an inflammatory phimosis, and the products of inflammation accu- 
mulate within the swollen prepuce. In some cases the prepuce be- 
comes gangrenous. 

Paraphimosis is produced by the retraction of a narrow prepuce 
behind the glans, with consequent stricture, inflammation, and some- 
times gangrene. 

Inflammation of the Corpora Cavernosa may be the result of 
injury, may follow fistulas, may occur in connection with inflamma- 
tion of the connective tissue of the pelvis, and may accompany the 
acute infectious diseases, such as pyaemia, small-pox, measles, ty- 
phus, etc. It may result in fibrous induration of portions of the cor- 
pora cavernosa ; in rare cases in abscesses or diffuse purulent infil- 
tration ; sometimes in gangrene. Tubercular inflammation of the 
penis has repeatedly followed circumcision performed by uncleanly 
tubercular persons. 

Syphilitic Ulcers frequently occur on the glans penis and pre- 
puce. The indurated chancre is formed either from an excoriation 
in which a pustule is formed or from a little nodule. The pustule 
breaks and its walls are infiltrated with small round cells. The 
nodule softens, breaks down, and forms an ulcer, of which the walls 
are infiltrated with cells in the same way. 

Syphilitic condylomata are of frequent occurrence on the glans. 

Phagedenic ulcers occur and may destroy a considerable part of 
the penis. Herpes of the prepuce occurs in the form of small vesicles^ 
which may later become ulcers. Erysipelatous and furuncular in- 
flammation sometimes involves the skin of the penis. 

TUMORS. 

Papilloma is found on the prepuce and glans penis. It occurs in 
the form of little warty growths, or of composite, cauliflower masses, 



744 THE ORGANS OF GENERATION. 

even as large as a fist. In either case the structure is the same — 
hypertrophied papillae covered with epithelium. Sometimes the epi- 
thelial layers become thick and horny, forming large, dense projec- 
tions. 

Fibroma diffusum, or elephantiasis of the prepuce, may occur, 
leading to immense thickening of the structure. It consists in a dif- 
fuse growth of the deep fibrous tissue of the cutis. Lipomata, 
angiomata, circumscribed fibromata, and sebaceous cysts may 
occur in the penis. Carcinoma of the penis usually occurs in the 
form of epitheliomata. These are most frequent in the prepuce and 
glans penis. They may have the form of flat ulcers, or of infiltrat- 
ing, ulcerating nodules, or very frequently assume the form of 
papillary outgrowths, which may attain great size, ulcerate, or un- 
dergo a variety of inflammatory changes. These growths may in- 
volve the entire skin of the penis ; they may invade deeper parts. 
The inguinal glands may be invaded. Distant metastases may occur, 
but are not frequent. 

Glandular carcinoma of the penis is not common. It may be sec- 
ondary to carcinoma in some other part of the body. 

Calcification and Ossification of the connective tissue of the 
corpora cavernosa sometimes occur. Large and small preputial cal- 
culi are occasionally found between the prepuce and the glans. 
These may be formed in situ, may come from the bladder or from 
without, and may later increase in size. 

THE SCROTUM. 

The skin of the scrotum is subject to the various forms of lesions 
which may occur in any part of the integument. 

Elephantiasis of the scrotum consists in the main of a develop- 
ment of new connective tissue from the cutis, which is sometimes ac- 
companied by dilatation of the lymph vessels. The thickened scrotum 
sometimes forms very large tumors, often rough upon the surface, 
which may entirely cover in the penis. Lipomata, fibromata, 
atheromatous or sebaceous cysts, and dermoid cysts containing 
hair, bone, cartilage, etc. , are sometimes found. Occasionally the 
skin of the scrotum is beset with numerous larger and smaller seba- 
ceous cysts, which raise the surface into little globular or wart- like 
projections. Epitheliomata, in the form of flat or papillary ulcerat- 
ing tumors, are of frequent occurrence among chimney sweepers, 
and may lead to extensive ulcerations of the adjacent parts and in- 
volvement of neighboring lymph nodes. 

Dermoids and Teratomata of the scrotum are not uncommon. 
In very rare cases tumors containing a considerable portion of a 
foetal skeleton have been found in the scrotum. 



! 



THE ORGANS OF GENERATION. 745 

THE TESTICLES. 
MALFORMATIONS. 

Absence of both testicles, either with or without absence of the 
epididymes, spermatic cords, and vesiculse seminales, occurs in rare 
cases. The scrotum is only indicated or may contain the epididymes. 
The penis is small, and the individuals are small and poorly de- 
veloped. 

Instead of being entirely wanting, the testes may be imperfectly 
developed. The individuals are weakly and effeminate. Absence 
of one testicle, with healthy development of the other, is more fre- 
quent. The corresponding epididymis and cord may be absent or 
present. 

The spermatic cords and vesiculse seminales may be absent or im- 
perfectly developed on one or both sides, while the testes are normal. 

Either one or both testicles may remain permanently in their 
foetal position, or may not descend into the scrotum for several years 
after birth (cryptorcliismus). Their descent may even be delayed 
until the thirtieth year of life. This condition may depend on an 
arrest of development in the testes or the gubernaculum testis ; on 
adhesions produced by intra-uterine peritonitis ; on narrowing of the 
inguinal canal ; on narrowing or shortening of the vaginal process 
of the peritoneum ; or on abnormal size or position of the testicle. 
Usually the malformation is confined to one testicle, and then is more 
frequent on the left side. The testicle is usually found in the abdo- 
men close to the mouth of the inguinal canal, or in the inguinal 
canal just below the external ring ; but it may be beneath the skin 
in the perineum, or in the crural canal with the femoral vessels, or 
elsewhere. The retained testis is usually not fully developed, or 
undergoes fatty or fibrous degeneration. The retention of one or 
-even of both testicles does not preclude the possibility of procreation. 
Retained testicles are prone to inflammatory changes and liable to 
become the seat of malignant tumors. 

Sometimes, while the testis is retained, the epididymis and sper- 
matic cord descend into the scrotum. In rare cases the position of 
the testis may be changed so that the epididymis and cord are in 
front. The existence of a supernumerary testis has been asserted in 
some cases, but is rather loubtful. 

Atrophy of the testicle may occur in old age or in persons who 
are in a condition of premature senility ; or as the result of pressure 
from herniee, hydrocele, or inflammatory products. 

HYDROCELE. 

Hydrocele of the tunica vaginalis consists in an accumulation of 






746 THE ORGANS OF GENERATION. 

serum in the cavity of this membrane. It is usually confined to one 
side. It is caused by acute or chronic inflammation of the tunica 
vaginalis, by varicocele, or by general dropsy. The serum is found 
in small or in large quantities ; it is usually transparent, may contain 
cholesterin, or be purulent and contain the pyogenic bacteria, or be 
mixed with blood. The tunica vaginalis remains unchanged, or is 
thickened, or contains plates of bone, or is covered with polypoid 
fibrous bodies which fall off and are found free in the cavity of the 
sac. There may be adhesions between the layers of the tunica vagi- 
nalis, and in this way the fluid becomes sacculated. The testis is 
pushed downward and backward ; it remains unchanged or is atro- 
phied. 

Hydrocele of the processus vaginalis consists in an accumulation 
of serum in the cavity of the vaginal process of the peritoneum, 
which remains open after the descent of the testicle. There are sev- 
eral different varieties. 

(a) The vaginal process is entirely open and there is a free com- 
munication with the peritoneal cavity. The serum may originate in 
the cavity of the peritoneum or of the vaginal process, and passes 
freely from one to the other. 

(b) The processus vaginalis is closed in the inguinal canal, while 
its lower portion is filled with serum. 

(c) The processus vaginalis is closed about the testis and the vis- 
ceral layer of the tunica vaginalis is formed. The serum accumu- 
lates in the upper part of the vaginal process which communicates 
with the peritoneal cavity. 

(d) The vaginal process is closed in the inguinal canal and over 
the testis ; the serum accumulates so as to form one or more sacs 
between these two points. Inguinal hernia may complicate this form 
of hydrocele. 

Hydrocele of the spermatic cord consists in a general oedema of 
the connective tissue of the cord, or in the development of circum- 
scribed cysts, in this connective tissue. 

A peculiar form of hydrocele is produced by the accumulation of 
serum in the sac of an inguinal hernia, from which the intestine has 
become retracted. 

HEMATOCELE. 

Hematocele of the tunica vaginalis consists in an effusion of 
blood into the cavity of this sac. It may be produced by injury ; in 
scurvy, or the hemorrhagic diathesis ; or it may complicate a pre- 
existing hydrocele. The effused blood usually soon degenerates, 
and we find the sac filled with a brownish fluid or a thick, grumous 
mass. The tunica vaginalis may be thickened. The testis remains 
normal or is atrophied. 



THE ORGANS OF GENERATION. 747 

Effusion of blood into the loose connective tissue of the scrotum 
is often called extravaginal hcematocele. 

Hematocele of the spermatic cord occurs in rare cases as a dif- 
fused infiltration of blood in the connective tissue of the cord. Or 
blood may be effused into a hydrocele of the cord. 

SPERMATOCELE. 

Cysts containing spermatic fluid not infrequently arise from the 
epididymis or from the rete testis. These sometimes acquire a 
large size and crowd the tunica vaginalis before them, so that they 
simulate a collection of fluid in the cavity of the latter. The wall of 
the cyst may be lined with ciliated or Avith flattened epithelium. 
The contents are sometimes simply serous, but more frequently opal- 
escent and contain great numbers of spermatozoa. 

INFLAMMATION. 

Inflammation of the testicles may be caused by injuries, exposure 
to cold, inflammation of the urethra, syphilis ; or it may occur in 
parotitis and in connection with various infectious diseases. The 
testes, epididymis, or tunica albuginea may be principally involved. 
Usually only one testicle is inflamed, sometimes both. The inflam- 
mation may extend to the vas deferens. The inflammation may be 
acute or chronic. 

Acute Orchitis is most frequent in the epididymis and tunica 
albuginea. When the testis is involved the organ is congested and 
infiltrated with serum or pus. From this condition it may return to 
the normal state ; or small abscesses may form which may be ab- 
sorbed, or they may increase in size so as to involve nearly the entire 
organ. They may perforate externally, and then healing may occur 
by means of granulation tissue ; or extensive gangrenous destruc- 
tion of the scrotum may occur. They may become enclosed in a 
fibrous capsule, and the contents dry and become cheesy or calcified, 
and so persist for a long time. The acute inflammation may pass 
over into the chronic form. Acute epididymitis is frequently the 
result of gonorrhceal infection, and may or may not be associated 
with inflammation of the testis. 

The products of inflammation may collect in varying quantity in 
the lumina of the seminiferous tubules and in the ducts of the epidi- 
dymis, and the epithelium of these structures may degenerate. 

Chronic Orchitis occurs as a sequel of acute inflammation or as 
an original condition. It may affect the testis, the epididymis, or 
the spermatic cord. The seminiferous tubules may be filled with des- 
quamated and degenerated epithelium ; they may be atrophied, or 
their walls may be greatly thickened so that they are converted into 



748 



THE ORGANS OF GENERATION. 



dense fibrous cords, with almost or quite complete obliteration of their 
lumina. There is usually a marked increase in the interstitial tissue, 
which causes atrophy of the tubules (Fig. 355). The albuginea may be 
greatly thickened. In some cases the testis is converted into a mass 
of dense connective tissue, in which but little trace of the original 
structure can be made out. The new-formed connective tissue may 
become calcified. A periorchitis may lead to thickening and union 
of the layers of the tunica vaginalis testis. Abscesses are not infre- 
quent in connection with chronic orchitis. 

Tubercular Orchitis may occur in connection with tuberculosis 




Fig. 355.— Chronic Interstitial Orchitis with Atrophy of the Seminiferous Tubules. 
a, thickened interstitial tissue; c, thickened merabrana propria of the tubules; d, separated 
epithelial cell mass in the lumen of the tubules. 

of the other genito-urinary organs or the lungs, in acute general 
miliary tuberculosis, or by itself. It usually begins in the epididy- 
mis and may extend from there to the testis, or it may commence in 
the testis itself. The appearances which the testicles present, when 
the seat of this form of inflammation, are exceedingly varied and 
difficult of interpretation. This is partly due to the complex struc- 
ture of the organ, partly to the varied complicating simple inflam- 
matory changes which the different parts of the organ undergo in 
connection with the special tubercular inflammation, and the impos- 






- 



THE ORGANS OF GENERATION. 



749 



sibility of making any definite morphological distinction between 
them. Further researches are urgently needed in this direction, and 
it seems probable that in the presence or absence of the tubercle 
bacillus we shall find the needed differentiating factor between va- 
rious inflammatory processes which are at present grouped under the 
general heading of tuberculosis testis. 

We may find in the testicle small circumscribed masses of cells, 
visible to the naked eye as whitish spots, which are sometimes com- 
posed of small spheroidal cells or of larger polyhedral or fusiform 
or round cells. These occur in the walls of seminiferous tubules and 
blood vessels, and in the interstitial tissue. Sometimes associated 
with these smaller nodules, and sometimes not, we find larger, ir- 
regular yellowish or gray cheesy masses, which are believed by many 
to be formed by the confluence and degeneration of the smaller 










1 



Fig. 356.— Chronic Orchitis with the Formation of Structures resembling Miliary Tubercles. 
a, thickened interstitial tissue; b, mass of granular cells in the interstitial tissue; c, thickened 
membrana propria of seminiferous tubule; d, mass of separated epithelium in tubule; e, accumula- 
tion of small spheroidal cells around tubules; /, thickened membrana propria enclosing g, a multi- 
nuclear mass resembling a giant cell. 

nodules. The cheesy masses may break down and open externally, 
giving rise to fistulas, gangrenous inflammation, etc. Hand-in-hand 
with this nodular formation of tissue, which is disposed to degenera- 
tive changes, there are various more or less diffuse alterations of the 
parenchyma and interstitial tissue of the organ which must not be 
overlooked, and which often constitute a most prominent and im- 
portant factor in the lesion. The interstitial tissue may be more or 
less densely and diffusely infiltrated with small spheroidal cells. The 
arteries are often the seat of obliterating endarteritis. The walls of 
the seminiferous tubules may be very much thickened, so that the 
lumen may be entirely obliterated. The epithelium lining the tubules 
may be fatty, disintegrated, and peeled off, or it may have largely 



750 THE ORGANS OF GENERATION. 

disappeared. The lumen of the tubules may be filled with a granular, 
nucleated mass which in transverse sections looks like a giant cell. 
The thickened walls of the tubules may be infiltrated with small 
spheroidal cells, so that the underlying stroma is scarcely visible. 
When this occurs in connection with a similar infiltration of the in- 
terstitial tissue and the formation of giant cells in the lumina, we 
have structures which present the greatest resemblance to some 
forms of tubercle granula (Fig. 356). 

Tubercular inflammation may extend from the testis to the vas 
deferens, vesiculse seminales, and prostate. 

Syphilitic Orchitis. — This may occur in the form of a diffuse 
new formation of connective tissue, which may occur in some par- 
ticular part of the organ or be widely distributed through it, and by 
reason of which the organ becomes dense and firm. Morphologically 
there is no difference between this form of orchitis and chronic in- 
durative orchitis from other causes. It may occur in children affected 
with congenital syphilis. Gummata may form in connection with 
the interstitial induration. These may disappear, leaving irregular 
cicatrices. 

Inflammatory foci in the testicle are common in leprosy. 

TUMORS. 

Fibroma occurs in the form of small dendritic or polypoid growths 
of the visceral layer of the tunica vaginalis. These sometimes be- 
come free and are found in the sac, usually in connection with hydro- 
cele. Small nodular fibromata occasionally occur in the albuginea 
and in the spermatic cord. 

Lipomata, either pure or in combination with myxoma and sar- 
coma, may arise from the connective tissue of the spermatic cord or 
from the tunica albuginea. 

Chondroma, sometimes in a pure form, but more frequently com- 
bined with myxoma and sarcoma, occurs in the testicles and may 
attain a large, size. Osteoma has been described. 

Sarcomata occur in the testes and epididymis, most frequently 
in the former. They present the greatest variety in structure. They 
may be composed of spheroidal or spindle-shaped cells ; they may be 
soft or contain much fibrous tissue ; they are very frequently com- 
bined with myxoma, chondroma, lipoma, etc. Owing to the occlu- 
sion of the seminiferous tubules, cysts may be formed in these sarco- 
mata. In these cysts polypoid growths of sarcomatous tissue may 
occur in the form of intracanalicular growths. Thus the so-called 
cysto-sarcomata of the testicle are formed. The walls of these cysts 
may coalesce, so that large, irregular cavities may be formed. When 
the cysts are not filled by polypoid outgrowths from their walls they 



. 



THE ORGANS OF GENERATION. 751 

may contain a mucous, serous, or bloody fluid, or masses of flattened 
cells, fat, and cholesterin. The cysts may be lined with cylindrical, 
ciliated, or flattened cells. 

Bhabdomyomata have been several times observed, frequently in 
combination with cysts. 

Adenoma is occasionally found, usually in combination with sar- 
coma or carcinoma, or with cyst formation. 

Carcinoma of the testicle is^ commonly of the soft medullary 
form, of rapid growth, and usually primary. It may commence in 
the testis or epididymis. Usually only one testicle is involved. Fre- 
quently the entire glandular portion of the organs is replaced by the 
new growth. The albuginea expands with the growth of the tumor, 
and may continue to enclose it even when of large size. The tissues 
are often very vascular, and haemorrhages, areas of softening, fatty 
and mucous degeneration are frequent. The inguinal and lumbar 
lymph nodes are apt to become involved, and distant metastasis may 
occur. Rarely the growth assumes a scirrhous form. 

Cysts. — Aside from the above-mentioned cysts which occur in 
connection with tumors and spermatocele, cysts may be formed from 
persistent remnants of Miiller's canal in the epididymis, or from ob- 
struction of the seminiferous tubules or ducts by inflammatory pro- 
ducts or tissue. 

Teratoid tumors of various kinds, with or without cysts, are of 
infrequent occurrence, and are sometimes quite complex in char- 
acter. They may be embedded in the substance of the gland. 1 
Probably some of the above-mentioned cystic rhabdomyomata be- 
long here. 

PARASITES. 

Echinococcus may occur in the testis or epididymis. 

THE SEMINAL VESICLES. 

The seminal vesicles may be the seat of acute or chronic inflam- 
mation, which is most frequently connected with inflammatory 
changes in adjacent parts, prostate, urethra, etc. As a result of 
chronic inflammation the vesicles may be atrophied, or they may be 
greatly dilated as a result of constriction of the ducts. 

Tubercular inflammation is usually secondary. Carcinoma of the 
rectum or other genito-urinary organs may secondarily involve the 
seminal vesicles. Small concretions, sometimes containing masses of 
permatozoa, are occasionally found in the seminal vesicles. 

THE PROSTATE. 

Hypertrophy of the prostate is a frequent senile change ; it is 
general or partial. 

Consult Wilms, Ziegler's Beitr. z. path. Anat., Bd. xix., p. 233, 1896. 



752 THE ORGANS OF GENERATION. 

In general hypertrophy the entire organ is enlarged and may 
reach the size of a man's fist. The enlargement is symmetrical, or is 
most marked in one half or in the so-called middle lobe. The organ 
is hard and dense, or soft or alveolar, containing numerous small 
openings from which a turbid fluid exudes. These different appear- 
ances depend upon the character of the hypertrophy. The muscular 
and fibrous tissue alone may be increased, which is most common, or 
at the same time the glandular tissue, or the glandular tissue alone. 
In the latter case the lesion is more properly an adenoma. The in- 
crease of muscular tissue properly constitutes a myoma. 

In partial hypertrophy we find circumscribed nodules of muscular 
tissue or of muscular and glandular tissue. They are usually situ- 
ated at the periphery of the organ and project into the bladder. 
They may become detached from the prostate, and are found as 
small, movable tumors beneath the mucous membrane of the blad- 
der. 

Both forms of hypertrophy frequently produce, by pressure, reten- 
tion of urine and changes in the bladder. 

Atrophy of the prostate is sometimes seen in connection with 
atrophy of the testicles, with castration, and as a result of inflamma- 
tion. Sometimes the ducts of the glandular portion are enlarged, or 
there may be fibrous degeneration of the organ. 

INFLAMMATION. 

Inflammation of the prostate is caused by gonorrhoea, by injuries, 
or, more rarely, is idiopathic. It may run an acute or chronic course. 
The gland may after a time return to its normal condition, or is grad- 
ually converted into a mass of fibrous tissue filled with abscesses. 
The abscesses may perforate into the bladder, urethra, vesiculse 
seminales, rectum, or peritoneum. Or the inflammation may extend 
to the connective tissue of the scrotum or beneath the pelvic perito- 
neum. The pus may become thickened and cheesy, or even calcified. 

Tubercular Inflammation of the prostate usually accompanies 
a similar lesion of some of the other genito-urinary organs, and 
is rarely of primary occurrence. Large cheesy masses are often 
formed, which may break down and open into the bladder or rec- 
tum. 

TUMORS. 

Adenoma of the prostate occurs in one of the forms of hypertro- 
phy of the gland, either with or without an increase in the fibro- 
muscular interstitial tissue. 

Carcinoma is of occasional occurrence, and may be primary or 
secondary. 



THE ORGANS OF GENERATION. 753 

Cysts of the prostate are sometimes found either as a result of 
occlusion of the ducts by hypertrophy of the interstitial tissue, tu- 
mors, etc. , or as a result of faulty development. 

PARASITES. 

Echinococcus of the prostate has been described, but is rare. 

CONCRETIONS. 

Small ovoidal or spheroidal, often brown or black bodies, having 
the characters of corpora amylacea, are of very frequent occurrence 
in the alveoli of the prostate, particularly in old persons. We find 
a certain number of them in the prostate of nearly all old men, but 
they are sometimes present in great numbers. Larger, irregular 
concretions, apparently formed by the coalescence or growth of the 
smaller ones, are less frequently found, and may be encrusted with 
lime salts. These concretions may give rise to ulceration of the 
ducts of the gland or to interference with the passage of urine, but 
in a majority of cases they seem to be of little or no practical impor- 
tance. 

cowper's glands. 

These glands may be enlarged and encroach upon the lumen of 
the urethra, either in acute or chronic inflammation. Cysts formed 
by the closure of the excretory ducts may also project into the ure- 
thral canal. 

THE MALE MAMMA. 

There may be an abnormal number of mammae. In boys, at 
about the time of puberty, the mammae may be swollen and inflamed 
or they may secrete milk. Cases are recorded in which adult males 
possessed large mammse which secreted milk. The breasts may be 
enlarged from an increase of fat or of connective tissue. 

Cysts of the male breast are not very infrequent. Fibromata, 
sarcomata, cysto-sarcomata, myxomata, and various forms of car- 
cinomata are recorded. 1 

1 For literature of tumor of male mamma see Gross, ' ' Tumors of the Mammary 
Gland," p. 237. 






THE BO^ES. 



DISTURBANCES OF CIRCULATION. 

Hypercemia. — The evidences of this condition are most marked 
to the naked eye in the periosteum and marrow, particularly the lat- 
ter. It should be remembered that the color of the marrow varies 
considerably under normal conditions, depending upon age and situ- 
ation. In the bones of the foetus and new-born, and near the areas 
of ossification in the young, the marrow is normally red in color. 
In adults the marrow of the sternum, vertebrae, and to a certain de- 
gree that of the ribs, pelvic and cranial bones, and the cancellous 
tissue of the ends of the long bones, is red or reddish in color. But 
most of the marrow, particularly in long bones of the extremities, is 
of a yellowish color from the presence of fat cells. In old age the 
marrow of all the bones is apt to become pale, and to assume a more 
or less translucent or gelatinous appearance. 

Hyperaemia usually occurs as an accompaniment of inflammatory 
processes in the bone, and, when marked, the periosteum is swollen 
and red ; the compact bone tissue may appear of a pink color, while 
the marrow, either by an increase in the amount of blood or absorp- 
tion of its fat, or both, may be of a uniform dark-red color or mot- 
tled with red and reddish-yellow. 

Hemorrhage. — This may be due to wounds and injuries, to in- 
flammatory and necrotic processes • and small haemorrhages often 
accompany scurvy, purpura, haemorrhagic diathesis, and leukaemia. 
Haemorrhages of considerable size between the periosteum and bone 
may lead to serious consequences, by cutting off the blood supply to 
the superficial layers of bone and thus inducing necrosis ; but when 
not in contact with the air they are not usually of serious import, since 
they are readily absorbed. The smaller haemorrhages of the medulla 
are not usually of much importance. The decomposition of the ex- 
travasated blood may lead to extensive pigmentation of the marrow. 

WOUNDS, FRACTURES, AND DISLOCATIONS. 

For details of the varied alterations produced under these con- 
ditions, and the secondary changes involved in the healing process, 



THE BONES. 755 

we refer to the section on repair, page 98, and to works on surgery. 
It may be stated here, however, that the healing of fractures occurs 
by the formation of granulation tissue in greater or less amount 
about the seat of fracture, and the direct formation of bone under 
the influence of osteoblasts, or by a preliminary formation of carti- 
lage or fibrous tissue and the gradual conversion of this into bone by 
metaplasia. 

INFLAMMATION. 

The periosteum, bone tissue, and marrow are so intimately con- 
nected that in most cases they all share to a greater or less degree in 
the pathological alterations of the bones. But as sometimes one, 
sometimes another is most markedly involved, it is convenient to 
consider separately here the inflammatory changes by which they 
are respectively affected. 

Periostitis. 

We may distinguish several varieties : 

1. Simple Acute Periostitis. — This form is apt to occur in chil- 
dren and ill-nourished persons from comparatively slight injuries or 
from unknown causes. The periosteum is thickened, succulent, 
congested, and more or less abundantly infiltrated with leucocytes, 
while the connective-tissue fibres are swollen. The periosteum be- 

' comes less firmly adherent to the bone, and the cells of the inner 
layers are increased in number. This variety of inflammation may 
terminate in the disappearance of the new elements and complete 
resolution, or it may represent a preliminary stage of one of the 
other varieties of inflammation. 

2. Suppurative Periostitis may begin as a simple or as a puru- 
lent inflammation. The pus is formed in the inner layers of the 
periosteum, and between it and the bone. The outer layers of the 
periosteum may resist for a long time the suppurative process. The 
accumulation of pus may dissect up the membrane from the bone 
and leave the latter bare. The pus thus formed may remain in this 
position for a long time, may be absorbed, may become dry and 
cheesy, or may burst through the periosteum and form abscesses in 
the soft parts. The bone, if separated from its nutrient membrane, 
may remain unchanged, but more frequently necrosis or inflamma- 
tion of the bone itself is set up. Such a periostitis may run an acute 
or a chronic course. 

Sometimes suppurative peritostitis takes on a very malignant 
character. Pus is developed not only beneath but in the periosteum, 
forming abscesses filled with foul pus. The periosteum, breaks down 
into a gangrenous, foul-smelling mass, and the, same change may af- 
fect the neighboring soft parts. The medulla may take part in the 






756 THE BONES. 

process and break down into a purulent, gangrenous mass. Hemor- 
rhages may complicate the process. The lymphatic nodes are en- 
larged and swollen ; abscesses may form in different parts of the 
body, and the patient may die with the symptoms of pyaemia. The 
pyogenic cocci may be found, under these conditions, in the exuda- 
tions of the periosteum as well as in the metastatic abscesses. 

3. Fibrous Periostitis. — This is a slow, chronic form of inflam- 
mation, resulting in the formation of new connective tissue in the 
periosteum, which becomes thickened and dense and unusually adhe- 
rent to the bone. It may be the result of necrosis, chronic arthritis, 
chronic ulcers of adjacent soft parts, etc. It may follow a simple 
acute periostitis. 

4. Ossifying Periostitis results in the formation of new bone 
from the inner layers of the periosteum. The masses of new-formed 
bone, called osteophytes, are of variable shape. They may form a 
thin, velvet-like, villous layer ; or they are little spiculse ; or they 
form larger, rounded masses, or a thick, uniform layer extending 
over a large part of a bone. They may be at first very loosely con- 
nected with the bone. The new bone has at first a loose, spongy 
character. It is formed of thin plates of bone enclosing large cavities 
filled with marrow. Layers of compact bone tissue are formed from 
the medulla on the sides of the original plates, and thus the medul- 
lary cavities are gradually filled up with bone. The new bone may 
thus become as compact or even denser than normal bone. The hyper- 
ostoses and exostoses thus formed may remain indefinitely, or they 
may gradually become smaller and finally disappear by absorption. 

The formation of new bone in the form of osteophytes, or in dense 
masses beneath and in the periosteum, occurs as a result of the same 
process by which bone tissue is normally formed. Certain rather 
large cells, called osteoblasts, which are formed along the blood 
vessels, possess the power of depositing osseous basement substance 
about themselves and so forming bone. Pathological new forma- 
tion of bone differs from the normal mainly in the conditions under 
which it occurs. The blood vessels around which the pathological 
bone develops, which grow out of the old vessels, as in the formation 
of granulation tissue, are irregularly arranged and subject to a variety 
of abnormal nutritive and mechanical conditions, so that the new 
bone is not usually formed in a series of definite systems of lamellse, 
but, as above described, in a series of irregular spiculae or masses. 
Moreover, as will be seen further on, the conditions under which it is 
formed being liable to change, and itself serving no definite purpose 
in the economy, as does normal bone, pathological new bone is often 
an evanescent structure. The details of its disappearance will be 



considered below. 



THE BONES. 757 

5. Syphilitic Periostitis. — Syphilitic poisoning may give rise to 
simple, purulent, fibrous, and ossifying periostitis. Or, in addition 
to these, gummy tumors may be developed in the periosteum. The 
bone tissue is usually more or less involved. The gummata may be 
absorbed or undergo cheesy degeneration, or be converted into fibrous 
tissue, or they may suppurate. 

6. Tuberculous Periostitis. — In badly nourished persons, particu- 
larly in children suffering from so-called scrofula (see page 528), a 
chronic purulent periostitis is frequently associated with the forma- 
tion of miliary tubercles. Abscesses are apt to form in and about the 
periosteum, and when these are evacuated granulation tissue may 
develop, in which miliary tubercles are formed. In these tubercles 
the Bacillus tuberculosis may be found. The bone is apt to be in- 
volved to a greater or less extent in the form of inflammatory changes 
or caries. 

Osteitis. 

Inflammation in bone tissue is dependent upon the same general 
conditions and presents essentially the same series of phenomena as 
inflammation in other kinds of connective tissue. But it is variously 
modified in detail by the peculiar dense and unyielding character of 
the basement substance, and by certain peculiarities of the blood 
supply and the nutritive conditions under which the cells are placed. 
In simple exudative inflammation the same series of phenomena 
occur in connection with the blood vessels, resulting in the production 
of serum, fibrin, and pus, as in other tissues ; but the extent to which 
these changes can occur is limited and constantly associated with 
striking alterations in the basement substance. It is these secondary 
alterations in the basement substance which lend to inflammations 
of the bone their most peculiar characters, and in the prominence 
which these assume the fundamental alterations are often overlooked. 
The most common of these secondary alterations are the absorption 
of the hard basement substance of the bone and its replacement by, 
or conversion into, young cellular forms of fibrillar connective tissue 
or marrow tissue, and the new formation, in more or less atypical 
manner, of new bone. As a result of these changes the bones in 
simple inflammation undergo alterations either in the direction of 
greater vascularity and increase of the spaces filled with granulation 
or marrow tissue, and so become more porous and less compact at the 
expense of the dense basement substance ; or they undergo alterations 
in the direction of an increase in density at the expense of new- 
formed or pre-existing marrow spaces. Or, as is frequently the case, 
both series of changes occur either simultaneously in different regions, 
or follow one another, or are variously associated together. Very 
frequently one or the other of the opposing forms of alteration pre- 
60 



758 



THE BONES. 



dominates, or one may occur to the exclusion of the other, and we 
thus have two prominent forms of inflammation, which are called 
rarefying osteitis or osteo-porosis, and condensing osteitis or 
osteosclerosis. The exact nature of the conditions under which in 
one case the bones become more, in another less dense, we do not 
understand. 

In addition to these phases of inflammation in bone, and in fre- 
quent and varied association with them, there are alterations leading 
to death and destruction of bone tissue in greater or less amount, 
which we call caries and necrosis ; and also inflammatory changes, 
more or less characteristic, due to the influence of peculiar specific 
agencies, such as the syphilitic and tuberculous infection, and we 




Fig, 357.— Rarefying Osteitis in Ulna of Child. 
a, isolated bone fragment with rough edges; b. marrow tissue; c, Howship's lacunae with 
osteoclasts. 

thus recognize tubercular and syphilitic osteitis. Again, the pro- 
duction of pus is so prominent a feature in some cases as to represent 
a purulent phase of the inflammatory process. Finally, any of these 
forms, and commonly several of them at, once, are variously asso- 
ciated with more or less marked inflammatory or degenerative alter- 
ations of the periosteum on the one hand, or the marrow tissue on 
the other, or of both combined. 

Rarefying Osteitis consists essentially in the formation in the 
marrow spaces, Haversian canals, or beneath the periosteum, of 
new, very cellular and vascular tissue, resembling granulation or 
young marrow tissue, in connection with which, or under whose 
influence, the basement substance of the bone is absorbed. The 



_.. 



THE BOXES. 759 

absorption of the bone occurs chiefly in the same way in which 
the bone is absorbed in normal growth, namely, under the influ- 
ence of certain large cells, called osteoclasts, which are grouped 
around the blood vessels. If we examine a thin section of bone 
which is undergoing absorption (Fig. 357), we find the edges of the 
bone which border on the vascular surfaces irregularly indented by 
deep or shallow depressions, sometimes simple, sometimes quite com- 
plex. These are called Hoic ship's lacunas and are usually filled or 
lined by larger and smaller granular, frequently multinuclear cells — 
the so-called osteoclasts. In the larger lacunae there may be granu- 
lation tissue with loops of blood vessels, with or without cells which 
have the morphological characters of osteoclasts. Under the influ- 
ence of these peculiar cells, or of the new vascular tissue, the bone 
is gradually absorbed. In other cases we find irregular branching 
channels through the bone across the lamellae, which appear to be 
due to the enlargement and coalescence of the lacunae and canaliculi, 
without the direct influence of blood vessels or other cells than the 
fixed cells of the bone. The tissue which replaces the absorbed bone 
may be very rich in small spheroidal cells, or it may be more or less 
fibrillar. As a result of this process irregular islets of bone tissue 
may be entirely separated from adjacent bone and surrounded by a 
more or less fibrillar vascular tissue ; this is most apt to occur in the 
cancellous tissue. Or the originally compact bone may become 
traversed by a series of larger and smaller irregular branching, com- 
municating channels with ragged walls. These progressive altera- 
tions may cease and be succeeded by a new formation of bone along 
the edges of the channels or cavities ; it may result in necrotic 
changes ; the vascular changes may become prominent and suppura- 
tion ensue. 

Rarefying osteitis may occur as an idiopathic disease from un- 
known causes ; it is often associated with the scrofulous diathesis, 
with diseases of the joints, with fractures or other injuries to the 
bone ; it often forms a predominant feature in tubercular inflamma- 
tion of the bones, etc. It is chiefly by a rarefying osteitis that bone 
tissue is eroded and destroyed in the vicinity of tumors, aneurisms, 
etc., which exert pressure on the bones. By the same process the 
sharp ends of fractured bones may be rounded off as healing pro- 
ceeds. 

When this form of inflammation occurs in cancellous bone tissue 
the marrow is red or gelatinous, and the bony septa may disappear 
altogether, so that in extreme cases we may have, instead of can- 
cellous bone, a mass of granulation tissue. When the disease occurs 
in the articular extremity of a bone the granulating medulla may 
send little offshoots through the articular cartilage. These may 



760 



THE BONES. 



become fused together and inflammation of the joint follow. The 
walls of the shafts of the long bones may be converted into spongy 
tissue. If, as is sometimes the case, an ossifying periostitis occurs 
at the same time, the bone is thickened but spongy ; or sometimes 
there are concentric layers of compact bone tissue, separated by rare- 
fied bone. 

Condensing Osteitis (Osteo-sclerosis). — This lesion is character- 
ized by the new formation of bone in the walls of the marrow cavi- 
ties or Haversian canals. The bone is formed under the influence of 
the blood vessels and osteoblasts, as in normal bone formation, but 
with less regularity. It may result in the conversion of cancellous 
tissue into compact bone, in the filling-up of the medullary cavity of 




«i'S*^- < '/t^^ -. Til 



Fig. 358.— Condensing Osteitis, or Osteo-sclerosis, of Ulna op Child. 
a, fragment of old bone with roughened, sinuous edges; 6, old Howship's lacunae covered with 
more recently formed bone lamellae. 

long bones with more or less dense bone tissue. The compact bone, 
owing to the filling of its Haversian canals, may become very dense 
and ivory-like. When the medullary cavities of long bones are in- 
volved the yellow marrow is converted into red marrow by the ab- 
sorption of fat and increased vascularity. It is frequently associated 
with ossifying periostitis. 

It very frequently follows rarefying osteitis, and under the micro- 
scope we can then often see the Howship's lacunao resulting from the 
original absorption process filled and covered in with new bone 
lamellae (Fig. 358). It is apt to occur in connection with necrosis or 
some chronic inflammation of adjacent soft parts, but it is sometimes 
idiopathic or occurs under unknown conditions. 



_ 



THE BONES. 



761 



Suppurative Osteitis (Abscess of Bone).— This process occurs 
usually in the ends of the long bones. It begins with a rarefying 
osteitis. The medulla undergoes actual suppuration, the bone tissue 
is destroyed, and a circumscribed cavity is formed in the bone, filled 
with pus and lined with granulation tissue. 

Less frequently abscesses are formed in the shaft of a long bone 
by a circumscribed suppuration of the medulla. These abscesses usu- 
ally occur in old people. They Jast for many years, have little ten- 
dency to perforation, may gradually enlarge and be accompanied by 
an ossifying periostitis, so that the bone is expanded. Very rarely 
acute suppurative osteitis, with rapid formation of an abscess, and 
perforation, has been observed. 




Fig. 359.— Tuberculous Osteitis. 
A miliary tubercle formed in the cancellous tissue near the joint in tubercular arthritis. 



In some cases, instead of abscess, there may be a diffuse infiltra- 
tion with pus of the Haversian canals or the spaces formed by rare- 
fying osteitis (see Osteomyelitis, page 763). 

Tuberculous Osteitis is essentially a rarefying osteitis associated 
with the formation of tubercle tissue and cheesy degeneration. The 
tubercles are sometimes small, scattered, and miliary in form (see 
Fig. 359); sometimes they unite to form larger and smaller masses. 
There may be extensive involvement of the medulla. There may be 
much simple granulation tissue or the formation of abscess associated 
with the process. Condensing osteitis and necrosis are not infre- 
quently present. Tuberculous osteitis is often associated with tuber- 
cular inflammation of the joints. It is most apt to occur in cancellous 



762 THE BONES. 

bone tissue, and is most common in the bodies of the vertebrae and 
in the carpal and tarsal bone. Tubercle bacilli may be found in the 
tuberculous masses, sometimes in considerable numbers. 

Syphilitic Osteitis. — The syphilitic poison may induce one of 
the above-mentioned varieties of osteitis, or it may produce gummy 
tumors. The gummatous osteitis usually commences in the peri- 
osteum, which becomes thickened and infiltrated with cells, so that 
there may be a circumscribed thickening of the periosteum, with 
or without distinct gummata. The vessels which extend from the 
periosteum into the bone become surrounded by new cellular tissue, 
which causes an enlargement of the canals. At this stage, if we 
strip off the periosteum, we drag with it the vessels surrounded by 
the new cell growth, leaving the bones beneath with numerous small 
perforations extending inward. As the disease progresses the gum- 
matous tissue around the vessels continues to increase, and the chan- 
nels in the bone enlarge by a rarefying osteitis and coalesce, form- 
ing large, irregular defects filled with gummatous tissue. In these 
masses of new tissue cheesy degeneration and the formation of 
fibrous tissue occur, giving them the characteristic appearance. In 
the vicinity of these gumma- filled spaces a condensing osteitis may 
occur, both in the substance of the bone and on the surface, in the 
form of osteophytes, so that the opening in the bone may be sur- 
rounded by an elevated, irregular ring of bone tissue. All this may 
occur beneath the uninvolved skin, or the skin may participate by a 
suppurative inflammation, resulting in ulceration. These processes 
may be circumscribed or involve a large part of a bone. It is not 
infrequently associated with necrosis of larger and smaller portions 
of bone. The gummatous tissue may be absorbed and its place be 
more or less filled with fibrous tissue. Syphilitic osteitis is most fre- 
quent in the cranial bones, but may occur elsewhere, as in the 
sternum, clavicle, tibia and fibula, the ribs, etc. 

Congenital Syphilis. — The bones of young children in this con- 
dition may occasionally show increased density or evidences of peri- 
ostitis, or irregular thickenings, particularly of the skull. The re- 
searches of Wegner, 1 which have been frequently confirmed by 
other observers, have shown that exceedingly characteristic changes 
very uniformly occur in the long bones in still-born or young chil- 
dren who are the victims of hereditary syphilis. These changes are 
found for the most part along the border zone between the epiphysis 
and diaphysis. It will be remembered that, in normal ossification 
of the long bones, the border line between the calcification and ossi- 
fication zones is narrow, sharply defined, and straight, or gently and 

1 Virchow's Arch., Bd. 1., 1870, p. 305. 



THE BOXES. 763 

evenly curved. In the syphilitic bones, on the contrary, this line 
is broader, uneven, and presents various modifications, depending 
upon the stage of the disease. Wegner distinguishes three promi- 
nent stages, which, however, merge into one another, so that all in- 
termediate forms may be seen. In the first stage there may be seen, 
between the cartilage and the new-formed spongy bone, a white or 
reddish-white zone, about two mm. in breadth, with very irregular 
borders, consisting of calcified cartilage, in which the linear groups 
of cartilage cells are more abundant than normal. In the second 
stage the calcified zone, still containing an unusual number of carti- 
lage cells, is broader and still more irregular and less sharply out- 
lined against the ossification zone. The cartilage just beyond it is 
softer and almost gelatinous, and may contain numerous blood ves- 
sels, islets of connective tissue or of calcification, or irregular ossifi- 
cation. In the third stage the bone may be pouched out at the sides 
around the ossification and calcification zones, and the perichondrium 
and periosteum thickened. The whitish, irregular calcified zone is 
hard and friable. Between this and the new-formed bone there is an 
irregular, soft, gray or grayish-yellow zone, from two to four mm. in 
thickness, which forms a loose, readily separated connection between 
the cartilage and the diaphysis. The white, friable zone consists 
mainly of irregular rows of degenerated and distorted cartilage cells 
lying in a calcified basement substance, of irregular masses of atypi- 
cal bone tissue, and of blood vessels surrounded by variously shaped 
cells. The soft zone consists of more or less vascular tissue with 
homogeneous basement substance, and round and spindle-shaped 
cells. This soft zone is not sharply outlined against the adjoining 
new-formed spongy bone, which, instead of consisting of the nor- 
mal marrow spaces with bony lamellae between them, is largely com- 
posed of granulation tissue. 

Different stages of this faulty development may be seen in differ- 
ent bones in the same individual. According to Wegner the lesion 
is usually most advanced in the lower end of the femur, then in the 
lower ends of the leg bones and of the forearm, then in the upper 
ends of the tibia, femur, and fibula. 

Not infrequently there is fatty degeneration of the marrow cells 
and blood vessels, giving the marrow a reddish-yellow color. These 
alterations of the bones may occur, not only in children who have 
gummata in other parts of the body, but also in those in which other 
evidences of syphilitic poisoning are absent. So uniform is their oc- 
currence that their presence alone suffices for the establishment of a 
diagnosis. 

OSTEOMYELITIS. 

In most of the inflammatory processes which affect the bones the 



764 THE BONES. 

medulla has an important share, so that many conditions described 
as osteitis are really osteomyelitis. It is customary, however, to 
reserve the latter name for these cases in which the medulla is pri- 
marily or chiefly involved. 

Acute Infectious Osteomyelitis. 

This may occur as the result of a local injury which permits the 
access or favors the development of pyogenic micro-organisms; it 
may be metastatic, resulting from the transportation of infectious 
material from other part of the body in septicaemia and pyaemia, 
in typhoid fever, in the exanthematous fevers, and under other con- 
ditions; or it may occur without evidence of local predisposition or 
of infectious processes in other parts of the body. 

The lesions of acute infectious osteomyelitis are, in the large 
majority of cases at least, due to the presence and action of the pyo- 
genic cocci, the Staphylococcus pyogenes and the Streptococcus 
pyogenes, and in many of its forms it may be regarded as one of 
the phases of septicaemia or septi co-pyaemia. 

While the lesions vary widely, the following general description 
is applicable to a considerable proportion of the cases : 

At the commencement of the disease, which usually begins in the 
shaft of one of the long bones, there is hyperaemia and oedema of the 
medulla, so that if the bone be opened the marrow is soft and of a 
dark-red color. A diffuse suppuration now rapidly ensues, and the 
marrow becomes streaked or mottled with gray. Occasionally, 
though not often, larger and smaller abscesses may form in the mar- 
row. The inflammatory areas may be circumscribed; or, in the 
more malignant cases, the entire marrow may become rapidly in- 
volved. The cancellous tissue of one or both of the epiphyses usually 
becomes involved. The disease, however, is not commonly confined 
to the medullary spaces. The periosteum becomes cedematous and 
infiltrated with pus, and the surrounding soft parts may become the 
seat of intense inflammatory changes. Abscesses of the periosteum 
or surorunding tissues are apt to form. As a result of these changes 
necrosis of greater or less portions of the bone may ensue. The 
medullary cavity may become enlarged as pus accumulates, and the 
wall of the bone may be broken through, permitting the discharge 
of pus outward. Sometimes several bones are involved at once. 
Secondary involvement of the joints is very frequent. There may 
be only a serous or purulent exudation ; or the acute and destructive 
inflammatory process may extend to the joint and produce extensive 
alterations. In young persons the epiphyses very frequently become 
separated from the shaft by the destruction of the cartilage which 
binds them together. 



THE BONES. 765 

In the severer cases, which are often denominated, par excel- 
lence^ malignant osteomyelitis, the changes may be very rapid and 
destructive. The medulla becomes broken down and gangrenous; 
the joints are soon involved; large portions of the bone, sometimes 
the whole shaft, necrose; the periosteum and surrounding parts be- 
come gangrenous; the veins contain thrombi, and pysemic infarc- 
tions and abscesses may form in various parts of the body. 1 

Chronic Osteomyelitis. — In the more chronic forms of osteomye- 
litis there is apt to be more or less ossifying periostitis and osteo- 
sclerosis, and fistulse may form in the bone, through which the exu- 
dations are discharged. 2 

NECROSIS. 

By necrosis we understand the death of a larger or smaller por- 
tion of bone. This condition is induced by causes which deprive the 
bone of its proper vascular supply from the periosteum and medulla. 
Suppurative periostitis, osteomyelitis, and osteitis, traumatic sepa- 
ration of the periosteum, ulcers of neighboring soft parts, emboli, 
the action of phosphorus vapor, and diseases, like typhus, which 
diminish the vitality, may cause necrosis. Necrosis is a pure form 
of gangrene, differing from gangrene of soft parts in that the dead 
bone has at first, and may retain for a long time, the general outward 
characters of the normal bone; while in dead soft parts the phenom- 
ena of decomposition, under the influence of bacteria, rapidly ensue, 
inducing marked complicating appearances in the dead, tissue. 

When a portion of bone has died an inflammation is set up at the 
dividing line between the dead and living bone. This inflammation 
has the characters of a rarefying osteitis (see above), and finally sep- 
arates the dead from the living bone. The dead bone, or seques- 
trum, may remain smooth and unaltered, or it may be eroded by the 
influence of surrounding pus or granulation tissue or osteoclasts. In 
this way it is possible for the sequestrum, if it be small, to be entirely 
absorbed. More frequently there is a production of new bone around 
the sequestrum, either beneath the periosteum or in the substance of 
the bone, and this becomes lined with granulation tissue, from which 
pus may continue to be formed, bathing the sequestrum. 

Necrosis may involve the superficial layers, or the entire thick- 

1 Consult for an elaborate treatment of acute osteomyelitis in its relationship to 
other forms of inflammation, with bibliography, Jordan, Beitr. z. klin. Chir., Bd. x., 
p. 587. For a study of this condition in childhood see Koplik and Van Arsdale, 
Am. Jour. Med. Sciences, April and May, 1892. 

2 For a resume of the deformities resulting from osteomyelitis consult Park, 
Medical Record, November 2d, 1895. 










766 THE BONES. 

ness of the wall of a long bone, or only the spongy tissue and inner 
layers of the wall, or an entire bone, or a number of different por- 
tions of the same bone, but it is most apt to occur in compact bone. 

The death and separation of the bone are very soon followed by 
the growth of new bone to repair the loss. The periosteum, the 
medulla, and the surrounding soft tissues may all take part in this 
new growth. The new bone is usually irregular, rough, perforated 
with openings through which pus formed around the sequestrum 
may be discharged. If the sequestrum be removed healing may oc- 
cur by the formation of new bone ; but the bone is usually more or 
less distorted by the irregular new ossification. 

Phosphorus Necrosis. — Under the influence of phosphorus vapor, 
periostitis and osteitis, particularly of the jaw, are apt to occur, 
which usually lead to more or less extensive necrosis, usually associ- 
ated with prolonged and often extensive suppuration. 

CARIES. 

Caries of bone is essentially an ulcerative osteitis resulting in pro- 
gressive molecular destruction of the bone tissue. It differs from 
necrosis in that, in the latter, larger and smaller masses of bone die, 
while in caries the destruction is molecular and gradual. It may 
occur in connection with any form of osteitis, with periostitis and 
osteomyelitis, or it may be secondary to inflammatory or destructive 
processes in the joints or adjacent soft parts. The depressed surfaces 
of bones in which caries is progressing are rough and more or less 
finely jagged, and may be covered with granulations. The minute 
changes by which ulceration and destruction of the bone are produced 
in caries are somewhat analogous with those in rarefying osteitis, 
but there are marked degenerative changes in the bone cells, which 
may become fatty or converted into a granular material. Moreover, 
the basement substance of the bone, instead of being absorbed, may 
disintegrate, with the formation of larger and smaller masses of 
detritus. Sometimes the lime salts are removed from the basement 
substance, which is converted into atypical fibrillar tissue and fatty 
and granular detritus. Very extensive suppurations and necrosis 
may be associated with caries. 

Long-continued caries, especially in badly nourished individuals, 
is apt to become complicated with tubercular inflammation. 

There is very little tendency to spontaneous healing in caries, but 
it may occur, and the defects produced may be more or less supplied 
by means of new-formed bone. 

RACHITIS (RICKETS). 

Rickets is a disease affecting the development of bone, prevent- 



- 



THE BONES. > 767 

ing its proper ossification. The disease usually occurs during the 
first two years of life, but may be congenital, 1 or may occur as late 
as the twelfth year. 

The physiological growth of bones depends upon three conditions. 
They grow in- length by the production of bone in the cartilage be- 
tween the epiphysis and diaphysis ; in thickness, by the growth of 
bone from the inner layers of the periosteum. At the same time 
the medullary canal is enlarged, in proportion to the growth of the 
bone, by the disappearance of the inner layers of bone. 

In rickets these three conditions are abnormally affected. The 
cartilaginous and subperiosteal cell growth, which precedes ossifi- 
cation, goes on with increased rapidity and exuberance and in an 





Fig. 360.— Rachitic Bone. 
Showing ossification zone in a longitudinal section of a rib. 

irregular manner, both between the epiphj^ses and diaphyses and 
beneath the periosteum, while the actual ossification is imperfect, 
irregular, or wanting. At the same time the dilatation of the me- 
dullary cavity goes on irregularly and often to an excessive degree. 
If we examine microscopically the region between the epiphysis 
and diaphysis (Fig. 360), we find that the cartilage cells are not reg- 
ularly arranged in rows along a definite zone in advance of the line 
of ossification, as in normal development, but that there is an irreg- 
ular heaping-up of cartilage cells, sometimes in rows, sometimes not, 
over an ill- defined and irregular area. The zone of calcification also, 
instead of being -narrow, regular, and sharply defined, is quite lack- 
ing in uniformity. Areas of calcification may be isolated in the re- 

1 Consult Salvetti, Ziegler's Bietr. z. path. Anat. , Bu. xvi., p. 29 (bibliography), 



768 THE BONES. 

gion of proliferating cartilage cells, or calcification may be altogether 
absent over considerable areas. 

Corresponding to these irregularities the ossification zone is also 
irregular. New-formed bone and marrow cavities containing blood 
vessels may lie in the midst of the cartilage, or masses of cartilage 
may lie deep in the region which should be completely ossified. In 
other places it seems as if the cartilage tissue were directly con- 
verted into an ill-formed bone tissue by metaplasia or direct trans- 
formation. It will readily be seen from this that the medullary spa- 
ces of the new-formed bone are irregular, and this abnormality is 
enhanced by the premature intramedullary absorption of the bone. 

The same sort of irregularity in the bone formation may be seen 
beneath the periosteum. An excessive proliferation of cells in the 
inner layers of the periosteum, the irregular calcification which oc- 
curs about them, and the absence of uniformity in the elaboration of 
ill-structured bone, conspire to produce an irregular, spongy bone 
tissue instead of the compact, lamellated tissue which is so necessary 
here for the solidity of the structure. The increased cell growth be- 
tween the epiphyses and diaphyses produces the peculiar knobby 
swellings which are characteristic of rickets. At the same time the 
medullary cavity increases rapidly in size and the inner layers of 
the bone become spongy. The medulla may be congested, and fat, 
if it has formed, may be absorbed, and a modified form of osteitis 
may ensue. 

The result of these processes is that the bones do not possess so- 
lidity and cannot resist the traction of the muscles or outside pres- 
sure. The epiphyses may be displaced or bent, especially in the ribs, 
less frequently in the long bones. The long bones and the pelvic 
bones may be bent into a variety of forms. Incomplete fractures 
are not infrequent. Complete fractures do not usually occur until 
the later stages of the disease, when the bones have become more 
solid. In the head, the cranium may be unnaturally large for the 
size of the face ; the f ontanelles and sutures may remain open ; the 
bones may be soft, porous, and hypersemic, while at their edges 
there may be rough, bony projections beneath the pericranium. 
Sometimes, especially in the occipital bone, there are rounded de- 
fects in the bone, filled only with a fibrous membrane ; this consti- 
tutes one of the forms of so-called craniotabes. 

It does not fall within the scope of this work to describe the vari- 
ous deformities which may occur as a result of this disease. The 
familiar pigeon breast ; the rows of knobs along the sides of the 
chest from bending and dilatation of the ribs at the point of junction 
of cartilage and bone ; the knock-knee, bow-legs, spinal curvatures, 
etc. , may all be the result of rachitic weakening of the bones. 



THE BONES. 769 

After a time the rachitic process may stop and the bones take on 
a more normal character. The porous bone tissue becomes compact 
and even unnaturally dense ; the swellings at the epiphyses disap- 
pear ; many of the deformed bones may become of a normal shape. 
In severe cases, however, the deformities continue through life ; es- 
pecially is there a cessation of the growth of the bones in their long 
axis, so that the persons affected are dwarfed. 

The disease may have an acute or a chronic character. The 
acute form begins usually during the first six months of life. The 
children are apt to suffer from vomiting, diarrhoea, profuse sweat- 
ing, chronic bronchitis and pneumonia, general anaemia, and wast- 
ing. They either die or the rachitic process is gradually developed. 
The chronic form is seen in older children, and often in those appa- 
rently healthy. The changes in the bones may take place without 
any constitutional symptoms, though there is often catarrhal bron- 
chitis, pneumonia, and anaemia. 

OSTEOMALACIA. 

This lesion consists in the softening of fully formed hard bone 
tissue by the removal of its inorganic salts. It is to be clearly distin- 
guished from rickets, whose lesions are due to a faulty development 
of bone, although in certain external characters the two diseases 
sometimes present considerable similarity. Osteomalacia usually 
occurs in adults, most frequently in females during pregnancy and 
after parturition ; more rarely it occurs in males, and in females un- 
associated with the above conditions. Its cause is not known. 

Microscopical examination shows that the decalcification occurs 
first in the periphery of the Haversian canals and in the inner layers 
of the walls of the marrow spaces. As the salts of lime are removed 
the basement substance at first remains as a finely fibrillated mate- 
rial, still preserving the original lamellation. The bone cells may be 
changed in shape or degenerated. After a time the decalcified tissue 
may disintegrate and be absorbed, and its place occupied by new- 
formed marrow or granulation tissue. As the disease goes on the 
marrow tissue is congested and red, the fat absorbed, and there is a 
great accumulation of small spheroidal cells ; or the marrow may 
assume a gelatinous appearance. The decalcification and absorption 
of the bone from within may proceed so far that the bony substance 
in the cancellous tissue almost entirely disappears, and the compact 
bone is reduced to a thin, soft, decalcified tissue. The disease is not 
always continuously progressive, but may be subject to temporary 
cessation. 

As a result of this softened condition of the bones, the weight 
of the body and the actions of the muscles may induce a series of 



770 



THE BONES. 



deformities which are sometimes excessive: curvatures of the spine, 
complete and incomplete fractures of the bone, distortions of the pel- 
vis, sternum, etc. There is a tendency in this disease to a general 
involvement of the bones, but the changes are sometimes confined to 
single bones or groups of bones. The cranium is rarely much 
affected. 






ALTERATIONS OF THE BONE MARROW IN LEUKAEMIA AND ANAEMIA. 

In certain forms of leukaemia the marrow of the bones is very 
markedly altered. The. change consists mainly in an accumulation 
in the marrow tissue of spheroidal cells, often in a condition of fatty 
degeneration, which lie in the meshes of reticular connective tissue 
and in and along the walls of the blood vessels. There may also be 
absorption of the fat, and sometimes enlargement of the marrow 
cavity from absorption of the bone. These alterations seem to be 
primarily due to an hyperplasia of the marrow cells. The new cells 
which accumulate in the marrow under these conditions are of vari- 
ous forms. Most characteristic are colorless, spheroidal cells which 
considerably resemble the large lymphocj'tes of normal blood (see 
page 82). But they are usually larger, though varying much in size, 
have one large, often vesicular nucleus staining less strongly than 
the lymphocyte nuclei, while the protoplasm usually contains neutro- 
phile granules (page 85). These cells are called myelocytes. In 
addition to these the marrow may contain, mingled with its usual 
elements, nucleated red blood cells, spheroidal cells containing red 
blood cells, and not infrequently considerable numbers of small octa- 
hedral crystals (called Charcot's crystals) . 

The degree to which this accumulation of cells varies much in 
different cases, and the gross appearances of the marrow are conse- 
quently very variable. In some cases the marrow is soft and has a 
uniform red appearance, or it is variously mottled with gray and 
red. Occasionally circumscribed haemorrhages are seen. In an- 
other class of cases, in which the cell accumulation is more excessive, 
the marrow may be gray, grayish-yellow, or puriform in appearance. 

These changes may occur in the central marrow cavity, as well 
as in the marrow spaces of the spongy bone. They may be present 
in several or many of the bones. They are usually accompanied by 
analogous changes in the spleen and lymph nodes. 

In certain cases of acute and chronic ancemia, particularly in the 
pernicious and progressive varieties, the marrow, especially of the 
larger long bones, may lose its yellow color from absorption of the 
fat, and become red. Microscopical examination of the marrow 
under these conditions may show myelocytes and sometimes an abun- 
dance of developing nucleated red blood cells and Charcot's crystals. 



1:1 



THE BONES. 7 71 

In many of the acute infectious diseases, typhus and typhoid 
fever, ulcerative endocarditis, recurrent fever, etc., the bone marrow 
has been found hypersemic and may, it is asserted by Ehrlich, con- 
tain myelocytes in increased numbers. 

All of these lesions of the marrow, although our knowledge of 
them is still very incomplete, together with what is known of the 
physiological functions of the marrow, point to a close relationship 
between the marrow and the spleen and lymph nodes as blood- 
producing organs. 1 

ATROPHY. 

In old age or in senile conditions the bones may become atrophied 
by the absorption of the hard tissue; the medullary spaces are en- 
larged, the marrow tissue contains less fat and is often gelatinous in 
appearance. As the result of the lack of use, or from any cause 
which interferes with the nutrition of the bone, such as paralysis of 
the muscles or diseases of the joints, the bones may atrophy. In 
connection with atrophy there may be an ossifying periostitis, 
which results in making the bone look even larger than normal. 
Many of the conditions commonly called atrophy, such as the erosions 
of bones from tumors, etc., pressing upon them, are really due to a 
rarefying osteitis. 

The bones, sometimes as the result of atrophy and sometimes 
from causes which we do not understand, are unusually brittle and 
liable to fracture. This disposition is sometimes hereditary. 

TUMORS. 

Tumors of the bone may involve either the periosteum, the com- 
pact bone, or the medulla, or, as is more frequently the case, two or 
more of these structures are involved at once. Tumors of the bone 
are usually accompanied by various secondary and sometimes very 
marked alterations of the bone tissue, osteoporosis, osteosclerosis, 
ossifying periostitis, etc. The new growths are very apt to undergo 
calcification and ossification. 

Fibromata may grow either from the periosteum or medulla. 
Their most common seat is in the periosteum of the bones of the head 
and face. They are apt to form polypoid tumors projecting into the 
posterior nares, pharynx, mouth, and antrum of Highmore. Cen- 
tral fibromata, i.e., those growing from the medulla, are rare. They 
usually occur in the lower jaw, but have been found in the ends of 
the long bones, the phalanges of the fingers, and the vertebrae. The 

1 The literature of the researches on the diseases of the spleen, which are impor- 
tant in this connection, may be found in part in Orth's "Lehrbuch der speciellen 
pathologischen Anatoinie, " Berlin, 1883, erste Lieferung, p. 119 et seq. 



772 THE BONES. 

fibromata may calcify or ossify, contain cysts, and not infrequently 
occur in combination with sarcoma. 

Myxomata are of occasional occurrence in bone. 

Osteomata. — New formations of bone as a result of inflammatory 
processes are, as we have already seen, of frequent occurrence in 
bone, and although not, strictly speaking, tumors, some of their 
forms are very closely allied to them, and they may therefore be con- 
veniently mentioned here. New growths of bone which arise from 
the surfaces are called exostoses or enostoses, according to their 
origin from the external surface or interior of the bone. They may 
contain all the constituents of normal bone : bone, medulla, vessels, 
periosteum, and cartilage. The new bone may be compact and like 
ivory, or spongy, or contain large cavities filled with marrow. 

The shape of exostoses varies greatly ; they may be in the form 
of sharp, narrow spiculae and processes, and, occurring in connection 
with periostitis, are called osteophytes. They may be polypoid in 
shape or form rounded tumors with a broad base. They may form a 
general enlargement of the bone, with much roughening of the sur- 
face ; this condition is often called hyperostosis. 

The bone beneath these new growths may be normal, or sclerosed, 
or rarefied, or the medullary cavity of the bone may communicate 
with that of the exostosis. Exostoses are usually developed from the 
periosteum, sometimes in the insertion of tendons and ligaments. 
They are very frequently multiple and may occur at all ages, even 
during uterine life. 

Enostoses are developed in the interior of bones from the medulla. 
They may increase in size, with absorption of the surrounding bone, 
until they project from the surface like exostoses. Their most fre- 
quent situation is in the bones of the cranium and face. 

Chondromata. — These tumors may be single or multiple, and 
most frequently grow from the interior of the bone, but sometimes 
from the periosteum. They are prone to form various combinations 
with other forms of tumors, as fibroma, myxoma, sarcoma, etc. 
They are frequently congenital, and are most common in young 
people. They occur most frequently in the bones of the hand and foot. 

There is a form of chondroma, called osteoid chondroma, which 
develops beneath the periosteum, most frequently in the femur and 
tibia near the knee joint, forming a club-shaped enlargement of the 
bone. The characteristics of the tissue composing these tumors are 
that it resembles somewhat the immature bone tissue which is seen 
beneath the periosteum in developing bone. It differs from carti- 
lage in the irregular shape of its cells, in the fibrillation and density 
of the basement substance, and in its general vascularity. On the 
other hand, it has not the inorganic contents or appearance of true 



THE BONES. 773 

bone. It resembles considerably the callous tissue forming about 
fractures of the bones. It may, however, and most frequently does, 
become converted, in some parts of the tumor, into true bone. On 
the other hand, combinations with sarcomatous tissue are of frequent 
occurrence (see below). 

Sarcoma. — This form of tumor is especially common in the 
bones. It grows from the inner layers of the periosteum or from 
the medulla, so that we may distinguish a periosteal and a mye- 
logenic sarcoma. Sometimes the tumor attacks the bone itself so 
early that it is impossible to say whether the tumor began in the 
periosteum or in the medulla. There is also a variety which grows 
close to the outside of the periosteum and becomes connected with it 
—par osteal sarcoma. 

The periosteal sarcomata usually belong to the varieties fibro-, 
myxo-, chondro-, and osteo-sarcoma, more rarely to the medullary 
variety. They commence from the inner layers of the periosteum, 
pushing this membrane outward. After a time the periosteum is 
attacked and the tumor invades the surrounding soft parts. The 
bone beneath may remain normal, or may be eroded and gradually 
disappear until the tumor is continuous with the medulla. Portions 
of the tumor may be calcified, or a growth of new bone may accom- 
pany its growth. The new bone usually takes the form of plates, or 
spiculsB, radiating outward. The minute anatomy of these tumors 
is very variable. The simplest — the fibro-sarcomata — are composed 
of fusiform, round, stellate, and sometimes giant cells (myeloplaxes), 
in varying proportions, packed closely in a fibrous stroma. In the 
medullary form the stroma is diminished to a minimum and the 
round cells are most numerous. In the chondro- and myxo-sar- 
coma the basement substance may be hyalin or mucous, and the 
cells follow the type of cartilage and mucous tissue more or less 
closely. There is a mixed form of tumor, called osteoid sarcoma, 
which is very apt to spread and to form metastases. The growth 
consists in part of tissue corresponding to fibro-sarcoma and round- 
celled sarcoma. In addition to this there occurs, in greater or less 
quantity, immature bone tissue, called osteoid tissue, which may in 
part become calcified, the calcification usually occurring in the cen- 
tral portions, leaving a softer peripheral zone. This form of tumor is 
most apt to occur at the ends of the long bones, and may form tumors 
of large size. It is often called, on account of its tendency to spread 
and to form metastases, malignant osteoma or osteoid cancer. 

Myelogenic sarcomata commence in the medulla and may grow 

rapidly. The bone surrounding them is destroyed and they project 

as rounded tumors. Most frequently new bone is formed beneath 

the periosteum, so that the tumor is enclosed in a thin, bony shell ; 

61 



774 THE BONES. 

sometimes there are also plates of bone in the tumor ; sometimes the 
periosteum is unaltered ; sometimes it is perforated and the tumor 
invades the surrounding soft parts. The tumors are frequently very 
soft, vascular, and hemorrhagic in parts, or may enclose cysts filled 
with tumor detritus and blood. They are usually of the spindle or 
round-celled variety, and not infrequently contain giant cells. 

The par osteal sarcomata resemble the periosteal, but they ap- 
pear to grow from the outer layers of the periosteum. They may 
be as firmly connected with the bone as the periosteal form. The 
periosteum may remain intact between the tumor and the bone, or 
it may disappear and leave them in apposition. 

Angiomata and Aneurism of Bone. — Avery large number of 
the tumors which have been described under these names are really 
sarcomata, or other tumors which happened to be very vascular. 
Some authors, indeed, are disposed to deny altogether the existence 
of real vascular tumors in bones. There are, however, reliable cases 
of cavernous angiomata growing between the periosteum and bone 
and intimately connected with the latter. Whether myelogenic an- 
giomata occur is doubtful. There are several cases described of 
cavities filled with blood in the interior of bones, which it is difficult 
to interpret. They have mostly been found in the head of the tibia. 
They are said to have consisted of single sacs composed of thickened 
periosteum, lined with plates of bone, and filled with fluid and clot- 
ted blood. No large vessels communicated with the sacs, but their 
walls were covered with a rich vascular plexus, branches of which 
opened into the cavity of the sac. 

Carcinomata. — Primary carcinomata are of very doubtful oc- 
currence in the bones. Most of the structures thus named have 
doubtless been sarcomata. Secondary carcinomata, on the other 
hand, as a result of metastases or local extension, are of not infre- 
quent occurrence and present various structural forms. Metastatic 
carcinomata may occur in the bones of various parts of the body at 
the same time, and are most apt to be secondary to carcinoma of the 
mamma. 

Cysts.— These most frequently occur in the maxillary bones, 
doubtless in connection with the teeth. They may be unilocular or 
multilocular, and contain clear serum or a mucous or brown fluid, 
and sometimes cholesterin. They may be lined with epithelium. 
They begin in the interior of the bone, and, as they increase in size, 
expand it until they may be covered with only a thin shell of bone. 
They may reach a large size, even as large as a child's head. 

Dermoid Cysts are occasionally found in connection with the 
bones, particularly of the skull. 



DISEASES OF THE JOINTS. 



For a description of the dislocations, misplacements, and injuries 
of the joints we refer to works on surgery. 

INFLAMMATION. 

Acute Arthritis. — The earlier stages of acute inflammation of 
ihe synovial membranes are better known from experiments on ani- 
mals than from post-mortem examinations. The first changes are 
swelling and congestion of the membrane, with increased growth 
and desquamation of epithelium, and infiltration of the membrane 
with lymphoid cells. These conditions are soon followed by an exu- 
dation. The exudation may be a clear serum, in which epithelial 
cells, lymphoid cells, and sometimes blood will be found. Or floc- 
culi of fibrin may float in the serum, or the fibrin may be in excess 
and the serum nearly absent. Or there is an excessive production of 
lymphoid cells, and the synovial sac is filled with pus. 

In Serous Arthritis the accumulation of serum within the syno- 
vial sac is the most prominent lesion. The disease may terminate in 
recovery, or become chronic, or pass into the suppurative form. It 
may be caused by contusions, penetrating wounds, gonorrhoea, rheu- 
matism, or it may occur without evident cause. 

Sero-fibrinous Arthritis may occur under the same conditions as 
those which lead to simple serous inflammation. The fibrin may be 
present largely as flocculi in the serum, or it may form false mem- 
branes over the surfaces of the joint. 

Purulent Arthritis may follow or be associated with the above 
forms of inflammation. The synovial membrane is thickened and 
cloudy, and there may be but a moderate amount of pus in the joint, 
and a slight degree of infiltration of the synovial membrane with pus 
cells. Under these conditions resolution may readily occur. 

In other cases the accumulation of pus in the cavity may be 
great, the synovial membrane and its surrounding tissue densely in- 
filtrated with pus cells. Under these conditions granulation tissue is 
apt to be found and the cartilages of the joints are apt to become 



776 DISEASES OF THE JOINTS. 

involved. There are swelling and proliferation or degeneration of the 
cartilage cells ; the basement substance becomes disintegrated, ulce- 
rates, and exposes the bone, in which osteitis, caries, rarefaction, 
etc., may occur. The new-formed granulation tissue may penetrate 
the cartilage, absorbing the basement substance, and by metaplasia 
the cartilage tissue may be converted into embryonal or granulation 
tissue. The pus may break through the capsule of the joint and 
form large abscesses in the adjacent soft parts. Sometimes the in- 
flammation is not only suppurative but gangrenous and runs a 
rapidly fatal course. The sjmovial membrane, articular cartilages, 
and ends of the bone all undergo a rapid suppuration and gangrene. 
Pyaemia and septicemia, small-pox, measles, scarlet fever, pneu- 
monia, gonorrhoea, 1 diphtheria, mumps, typhus fever, glanders, the 
puerperal condition, exposure to cold, penetrating wounds, and in- 
juries, may all give rise to or favor the development of purulent 
synovitis. 

Chronic Arthritis may begin as such or it may be the result of 
previous acute inflammation. There is an increase of fluid in the 
joint. This fluid is thin and serous, or is thickened with flocculi of 
fibrin and epithelial and lymphoid cells, or is thick, syrupy, or even 
gelatinous. The synovial membrane is at first congested, its tufts 
prominent. Later it becomes thickened, sclerosed, and anaemic ; the 
epithelium is destroyed and the tufts become large and projecting. 
From the distention of the capsule there may be subluxations or lux- 
ations of the joint, or the capsule may be ruptured. 

Chronic Rheumatic Arthritis is most common in elderly per- 
sons, usually affecting several joints and advancing slowly and 
steadily. There is a chronic thickening of the synovial membrane 
and the fibrous tissue adjacent to it. Fluid accumulations are not 
common. The articular cartilages are apt to degenerate or ossify, 
or become softened and fibrillated, and they may disappear. The 
contracting synovial membranes and fibrous tissue render the joints 
stiff and may cause considerable deformity. Not infrequently fibrous 
and bony anchyloses are formed between the ends of the bones. 

Arthritis deformans. — This name has been applied to a variety 
of chronic inflammation of the joints which, combined with degene- 
ration of parts of the joint and the new formation of bone, may re- 
sult in marked deformities of the part. 

It usually occurs in elderly persons and is apt to involve several 
joints, most frequently the hip, knee, fingers, and feet. It may be 
idiopathic, or due to rheumatism or to injuries, or follow an acute 
arthritis. The capsules of the affected joints are thickened and scle- 

1 For discussion of gonorrheal arthritis consult JVorthrup, Trans. Assn. Am. 
Phys., vol. x., p. 141, 1895 



DISEASES OF THE JOINTS. 777 

rosed. The synovial fluid is at first increased in quantity; later, 
diminished and thickened. The tufts of the synovial membrane be- 
come much enlarged and vascular ; they may be converted into 
cartilage. Sometimes the capsule becomes ossified. The new bone 
grows from the edge of the cartilage within the capsule and its 
articular surface is covered with cartilage. The articular cartilages 
are much changed. The basement substance splits into tufts, while 
the cartilage cells are increased in number. Or the basement sub- 
stance becomes fibrous ; or it is split into lamelh© and the cartilage 
cells are multiplied ; or there is fatty degeneration and atrophy. 

As a result of these changes larger or smaller portions of the 
cartilage are destroyed and the bone beneath is laid bare. The ex- 
posed bone may become compact and of an ivory smoothness. The 
ends of the bones are much deformed. They are flattened and made 
broader by irregular new growths of bone, while at the same time 
they atrophy. The new growth of bone starts from the articular 
cartilages. The cartilage cells increase in number and the basement 
substance in quantity. This growth is most excessive at the edge of 
the cartilage, so that a projecting rim is formed there. This pro- 
jecting rim may ossify next the bone, and at the same time new carti- 
lage may form on its surface, so that we may find large masses of 
Done covered with cartilage. All these changes occur in various 
combinations and sequences, so that joints in this condition present 
the greatest variety of appearances. 

Arthritis uritica (Gouty Arthritis). — This disease is character- 
ized by the deposit of salts of uric acid in the cartilages, bones, and 
ligaments, and also in the cavities of joints. The deposits may be 
in the form of stellate masses of acicular crystals in and about the 
cartilage cells or in the basement substance ; or they may be deposited 
in the fibrillar connective-tissue structures of the joint in single crys- 
tals, or in the subcutaneous tissue about the joint as white concre- 
tions. The deposits may occur in repeated attacks of the disease, 
and are accompanied by acute inflammatory changes. They may 
lead to various forms of chronic inflammation of the joints. 

Tuberculous Arthritis (Chronic Fungous Arthritis ; Strumous 
Arthritis). — This disease may commence in the joint itself, or be 
transmitted to it from a tubercular inflammation of the bone. It is 
characterized by the formation of granulation tissue containing 
tubercles, sometimes in great quantity, and usually associated with 
secondary inflammatory and degenerative changes of surrounding 
parts. According to the prominence of one or other of these second- 
ary alterations, several forms of tubercular arthritis may be dis- 
tinguished. If there is an excessive growth of granulation tissue 
without much suppuration, this constitutes a fungous form. Some- 



778 DISEASES OF THE JOINTS. 

times there is extensive suppuration, so that the cavity of the joint 
may be filled with pus, which may be discharged through openings 
in the skin ; or there may be more or less extensive formation of 
abscesses, or infiltration of the soft parts about the joint with pus. 
In other cases there is a predominant tendency to breaking-down of 
the new-formed tubercular tissue and of the tissues of the joint — 
ulcerative form. The cartilage basement substance may become 
split into fragments and the cells degenerate, and thus deep and de- 
structive ulcers of the cartilage be formed. Or the granulation tissue 
may work its way through the cartilage into the bone beneath, by 
absorption of the basement substance of the cartilage, with or with- 
out proliferation of its cells. Caries and necrosis of the underlying 
bone may lead to extensive destruction. Hand-in-hand with these 
alterations subperiosteal new formation of bone may occur, or sclero- 
sis of the adjacent bone tissue. There may also be a great increase 
of fibrous tissue about the joint. Tubercle bacilli may be found in 
the tubercular tissue and in the exudations. 

This disease is most common in children and young persons. The 
so-called scrofulous diathesis is said to predispose to it, but local 
injuries are frequently the predisposing factors. It is most common 
in the large joints. It may occur in connection with tubercular in- 
flammation in other parts of the body, but it is frequently quite 
local, and may remain so for a very long time or permanently, since 
general infection from tubercular arthritis is comparatively infre- 
quent. 

The disease always runs a very chronic course and may destroy 
the patient's life. If recovery takes place before the cartilages and 
bones are involved the joint is preserved ; but it may be stiffened, or 
even immovable, from the contraction of the new fibrous tissue 
around it. If the cartilages and bones are diseased the joint is de- 
stroyed, and either bony or fibrous anchylosis results. Sometimes 
from the change in the articulating surfaces, and the contraction of 
the muscles and the new fibrous tissue, partial or complete disloca- 
tions are produced. 

Occasionally miliary tubercles occur in the synovial membranes 
in cases of general miliary tuberculosis, with but little accompanying 
simple inflammatory change. 

TUMORS. 

Secondary tumors of the joints as a result of local extension from 
the adjacent parts are not uncommon, and the tumors may be of 
various kinds. Primary tumors of the joints, on the contrary, are 
not very common. 

Lipoma. — A new growth of fatty tissue may begin in the other 



DISEASES OF THE JOINTS. 779 

portions of the synovial membrane, push this inward, and project 
into the joint in a mass of tufts — lipoma arborescens. 

Fibroma occurs as an hypertrophy of the little tufts and fringes 
of the synovial membrane. In this way large polypoid and dendritic 
bodies are formed. The pedicles of these growths may atrophy and 
even disappear, so that the growths are left free in the cavities of the 
joints. 

Corpora aliena Articulorum (Loose Cartilages in the Joints). — 
This name is given to bodies, of various structure and origin, which 
are found free or attached by slender pedicles in the cavities of the 
joints. They are most frequently found in the knee ; next in order 
of frequency in the elbow, hips, ankle, shoulder, and maxillary joints. 
They may be single or in hundreds. Their size varies from that of 
a pin's head to that of the patella. They are polypoid, rounded, egg- 
shaped, or almond-shaped ; their surface is smooth or faceted, or 
rough and mulberry-like. They are composed of fibrous tissue, car- 
tilage, and bone in various proportions. 

These bodies are formed in different ways. 

1. By hypertrophy of the synovial tufts and production of car- 
tilage and bone in them. 

2. More frequently by a change into cartilage of portions of the 
synovial membrane. Small, flat plates of cartilage form on the inner 
surface of the synovial membrane, and these increase in size and 
their outer layers ossify. They may remain fixed in the synovial 
membrane ; or they project and become detached from it, and they 
then appear as flattened, concave bodies composed of bone covered 
with cartilage on one side. 

3. The growth of cartilage and bone begins in the outer layers of 
the synovial membrane or in the periosteum near the joint. The new 
growth pushes the synovial membrane inward, and projects into the 
joint as a polypoid body covered with the inner layers of the synovial 
membrane. Later the membrane atrophies and the growth becomes 
free in the joint. 

4. There may be cartilaginous outgrowths from the edges of the 
articular cartilage. 

5. Rarely portions of the articular cartilages may be detached by 
violence or disease ; or fibrinous and other concretions may result 
from arthritis, or under conditions which we do not understand. 






MUSCLE. 



LESIONS OF VOLUNTARY STRIATED MUSCLE. 

Haemorrhage. — This may occur as a result of mechanical injury ; 
from rupture of the fibres by convulsive contraction, as in tetanus ; 
or it may occur when the muscle fibres are degenerated, as in typhoid 
fever ; or in connection with certain general diseases, as scurvy, 
purpura, haemorrhagic diathesis, septicaemia, etc. The blood is usu- 
ally readily absorbed. 

Embolic Infarction of Muscles in connection with heart dis- 
ease has been described in a few cases, but it is rare. 

Wounds and Rupture. — When the muscle fibres are severed by 
wounds or rupture there is more or less degeneration of the divided 
fibres, and the wound may heal by the production of granulation tis- 
sue, which gradually becomes converted into cicatricial tissue, thus 
binding the severed parts together. In some cases there is a new 
formation of muscle fibres, which penetrate the cicatrix and establish 
muscular connection between the parts. When the wound does not 
gape, so that the severed ends are not much separated, there may be, 
it would seem, a direct re-establishment of muscular continuity by 
new development of muscle, without the formation of much new con- 
nective tissue. 

The exact way in which muscle fibres are regenerated is yet 
somewhat uncertain. In many cases there seems to be a prolifera- 
tion of the so-called muscle corpuscles, leading to the formation of 
elongated cells or strings of cells, which are gradually converted into 
striated muscle. In some cases the appearances would seem to in- 
dicate that connective-tissue cells may participate in the formation of 
new muscle fibres, but this is not certain. 1 

INFLAMMATION. 

Suppurative Myositis. — In the early stages of this lesion we 

1 For literature on muscle regeneration consult Zaborowski, Arch, f iir exp. Patho- 
logie u. Pharm., Bd. xxv., Heft. 5 und 6, p. 415, 1889. 



MUSCLE. 781 

find the muscle hyperaemic and (edematous, and the interstitial tis- 
sue more or less infiltrated with small spheroidal cells, doubtless the 
result of emigration. If the inflammation becomes intense there 
may be an excessive accumulation of pus cells, either diffusely in the 
interstitial tissue or in larger and smaller masses. Hand-in-hand 
with this cell accumulation occur degenerative changes in the mus- 
cle fibres. By pressure their nutrition is interfered with and they 
undergo granular, fatty, or hyalin degeneration. They may com- 
pletely disintegrate and gangrene may occur, so that larger and 
smaller masses of the infiltrated muscle tissue become soft, foul- 
smelling, and converted into a mass of detritus in which but little 
muscle structure can be detected, and which is intermingled with 
bacteria. In other cases there may be larger and smaller abscesses 
formed in the muscle, the muscle tissue itself either degenerating and 
disintegrating and mixing with the contents of the abscess, or being 
pressed aside and undergoing atrophy and degeneration. In some 
cases, when the formation of pus is moderate in amount, there may 
be restoration by formation of granulation tissue between the muscle 
fibres. This becomes gradually dense and firm, and leads to more or 
less atrophy of the muscle fibres by pressure. 

Acute suppurative myositis may accompany wounds ; it is very 
common in acute phlegmonous inflammations of the skin and subcu- 
taneous tissue, and often accompanies acute infectious diseases, such 
as pyaemia, erysipelas, etc. In most cases the pyogenic bacteria are 
present in the inflammatory foci. It is not infrequently seen in the 
muscles adjacent to the inflamed mucous membranes in diphtheria. 

Chronic Interstitial Myositis. — In this lesion there is a new 
formation of connective tissue between the muscle fibres or bundles of 
fibres. This new tissue is sometimes very cellular, resembling gran- 
ulation tissue, and this probably represents an early stage of the 
disease. In other cases (Fig. 361) we find dense cicatricial tissue 
crowding the muscle fibres apart, inducing atrophy in them, and 
sometimes causing their complete destruction. This lesion, which is 
the analogue of chronic interstitial inflammation of the internal 
organs, may occur in muscles which are adjacent to other parts which 
are the seat of chronic inflammatory processes. It may occur in 
muscles which are not used. The new formation of connective tissue 
would in some cases seem to be secondary to atrophy of the muscle 
fibres. In this case it would more appropriately be called replace- 
ment fibrous hyperplasia. 

Myositis ossificans. — Under conditions and for reasons which 
we do not understand, there occasionally occurs, usually in young 
persons, a new formation of bone tissue in the interstitial tissue of 
muscles, in the tendons, ligaments, fasciae, and aponeuroses. This 



782 



MUSCLE. 



sometimes apparently starts as outgrowths from the periosteum, 
sometimes not. The bone formations are apt to commence about the 
neck and back, and may become very widespread over the body. So- 
far as the muscles are concerned, there is usually an increase of con- 
nective tissue between the fibres and bundles, in which new bone is 
formed, usually in elongated and sometimes in spicula-like masses. 
The muscle fibres undergo secondarily a greater or less degree of 
atrophy or degeneration. There may be fatty infiltration between the 




Fit*. 361.— Chronic Interstitial Myositis. 
The connective tissue is dense in texture, and the muscle fibres are atrophied and partially 
destroyed. 



fibres, and various deformities are produced by the shortening and 
progressive immobility of the affected parts. * 

While the above disease is a progressive and frequently a general 
one, there may be new formation of bone in muscle as a result of pro- 
longed or repeated mechanical irritation. Thus in the adductors of 
the thigh in persons who are constantly in the saddle, or in the del- 
toid muscle of soldiers who strike this part with their weapons in 
drill, there may be a formation of bone. 

Gummata and occasionally tubercles occur in the connective tis- 
sue of muscle. 

1 The literature of Myositis ossificans may be found, together with a description of 
some interesting cases, in an article by Mays in Virch. Archiv, Bd. Ixxiv., p. 145. 



MUSCLE. 



783 



DEGENERATIVE CHANGES IN THE MUSCLES. 

Simple Atrophy. — This may occur in old age, in prolonged ex- 
hausting diseases, or as a result of pressure from a foreign body, 
tumors, etc. The muscle fibres grow narrower, the degree of narrow- 
ing frequently varying considerably in different parts. They usually 
retain the striations, but these may be obscured by degenerativo 
changes. The sarcolemma may become thickened, and there may 
be a considerable increase in connective tissue between the muscle 
fibres and bundles. 

Progressive Muscular Atrophy. — This lesion consists essentially 
in a combination of simple or degenerative atrophy of the muscle 
fibres with chronic interstitial inflammation, and is sometimes associ- 
ated with proliferative changes in the muscle nuclei. In the earlier 



4 





Fig. 362.— Progressive Muscular Atrophy (Soleus muscle, longitudinal section). 
a, atrophied muscle fibre; 6, degenerated muscle fibre; c, interstitial tissue; d, clusters of pro- 
liferated muscle nuclei. 



stages of the disease the muscles may be pale and soft, but exhibit 
otherwise to the naked eye but little alteration. Gradually, however, 
the muscle substance becomes replaced by connective tissue, so that 
in marked and advanced cases the muscles are converted into fibrous 
bands or cords, whose cicatricial contraction may induce great de- 
formities. 

Microscopical examination shows in the early stages of the disease 
a proliferation of cells in the interstitial tissue, so that this may have 
the appearance of granulation or embryonal tissue ; also in some 
cases marked proliferative changes in the muscle nuclei (Fig. 362), 



784 



MUSCLE. 



leading to the formation of new cells which may more or less replace 
the contractile substance within the sarcolemma. The new inter- 
stitial tissue increases in quantity and grows denser, and may crowd 
the muscle fibres apart (Fig. 363). The walls of the blood vessels 
may also become thickened. Hand-in-hand with these interstitial 
alterations the atrophy of the muscle fibres proceeds. These may 
simply grow narrower, retaining their striations ; or they may split 
up into longitudinal fibrillae, or transversely into discoid masses, and 
in this condition disappear. In other cases a certain amount of 
fatty or hyalin degeneration may be present. These degenerative and 




Fig. 363.— Progressive Muscular Atrophy (Soleus muscle, transverse section). 
a, increased interstitial tissue; 6, nearly normal muscle fibres; c, degenerated muscle fibres; 
d, atrophied muscle fibres; e, clusters of proliferated muscle nuclei. 

proliferative changes do not, as a rule, occur uniformly in the affected 
muscles, but some parts are affected earlier and more markedly than 
others. The atrophied muscle may be replaced by fat. 

Progressive muscular atrophy is apt to commence in the small 
muscles of the extremities, in many cases in the muscles of the ball 
of the thumb. It may commence in the muscles of the shoulder, 
the arms, or the back. It may have a continuous extension, or it 
may jump single muscles or groups of muscles. Death may be in- 
duced by the affection of the muscles of respiration or deglutition. 

The causes of this lesion are in many cases unknown, and there 



MUSCLE. 



785 



is considerable lack of unanimity of opinion as to whether it is pri- 
marily a disease of the muscles or of the nervous system. In a 
considerable proportion of cases the muscle lesion is associated with 
atrophy of the ganglion cells in the anterior cornua of the spinal 
cord and the development of connective tissue about them. In 
other cases these changes in the cord may apparently be absent. 

It is sometimes accompanied by atrophy of the nerves which are 
distributed to the muscles, and atrophy of the anterior roots has 
been described. 

It is probable that there are several varieties of progressive mus- 
cular atrophy, which our present knowledge does not enable us to 




Fig. 364.— Pseudo-hypertrophy of Gastrocnemius Muscle (Fatty Infiltration). 
The specimen is from the case mentioned below, accompanying multiple neuroma. 

clearly distinguish. Muscular atrophy in some cases follows over- 
straining of groups of muscles, or injuries, and may occur as one 
of the sequelae of typhoid fever and diphtheria. 

Atrophia Musculorum lipomatosa (Pseudo-hypertrophy of the 
Muscles). — In some cases, hand-in-hand with the production of new 
connective tissue in the muscles and the atrophy of the muscle 
fibres, or after these changes have made considerable progress, there 
occurs a development of fat tissue between the fibres (Fig. 364) which 
may prevent any apparent diminution in the size of the muscles, or 
in some cases may even give them a great increase in size. This condi- 



~ 






?86 MUSCLE. 

tion is of most frequent occurrence in children, and is most apt to 
appear in the gastrocnemii muscles. In the upper extremities the 
deltoid and triceps are most frequently involved. The lesion may be 
symmetrical, affecting similar muscles on both sides of the body, or 
it may be unilateral. Parts of muscle bellies may be affected. 

The cause of this form of atrophy is not definitely known. Vari- 
ous lesions of the spinal cord have been described as occurring with 
it ; • but, in many cases at least, alterations of the nervous system 
cannot be detected. The writer has described a case 1 in which this 
lesion was marked in the gastrocnemii in connection with multiple 
false neuromata. 2 

Fatty Degeneration, with greater or less destruction of the mus- 
cles, may commence with a simple swelling and fine granulation of 
the fibres. As the process goes on, smaller and larger fat droplets 
appear in the contractile substance, which loses its striations and 
becomes friable, and may be entirely destroyed, leaving within the 
sarcolemma a mass of fatty detritus which may finally be absorbed 
and disappear. This alteration may occur in acute parenchymatous 
myositis in connection with various forms of atrophy, in prolonged 
exhausting diseases, and in phosphorus poisoning. 

Hyalin Degeneration. — Under a variety of conditions the mus- 
cle fibres undergo a peculiar series of changes, leading to their con- 
version into a translucent, highly ref ractile material, somewhat re- 
sembling amyloid but not giving its micro-chemical reactions, and 
apparently more nearly allied to the material produced in the so- 
called hyalin degeneration. The lesion in the muscle which we 
are considering is commonly called waxy degeneration, from the 
peculiar appearance which the muscles present. When the lesion is 
far advanced and extensive the muscles are brittle and have a gray- 
ish-yellow, translucent appearance. Microscopical examination of 
various stages of hyalin degeneration of muscle shows that the con- 
tractile substance of the fibres becomes at first swollen and granular, 
and gradually converted into hyalin material which may present 
the outlines of the swollen fibres, but is more frequently broken into 
larger and smaller shapeless clumps (Fig. 365), which may disin- 
tegrate and finally be absorbed. Hand-in-hand with these changes 
there usually occurs an increase in the interfibrillar connective tissue, 
and in certain cases there may be a proliferation of the muscle nuclei 
and a new formation of variously shaped cells within the sarco- 

1 Prudden, American Journal of Medical Sciences, July, 1880, p. 134. 

2 For bibliography of muscular atrophy consult Friedreich^ "Ueber progressive 
Muskelatrophie," etc., Berlin, 1873 ; also " Dictionnaire encyclopedique des Sciences 
medicales,"2ser., i., x. ; or Eulenberg's " Real-Encyclopadie der gesammten Heil- 
kunde," article by Pick on Muskelatrophie. 



MUSCLE. 



787 



lemma which leads to the regeneration of the fibres. As a result of 
the brittleness of the degenerated muscles they are apt to rupture, 
and in this way haemorrhage may occur. 

This form of degeneration may occur in progressive muscular 
atrophy, in variola, cerebro-spinal meningitis, trichinosis, in connec- 
tion with inflammation, injuries, freezing, etc. It is, however, most 
marked and frequent in typhoid fever. In this disease the rectus 
abdominis and the adductors of the thigh are most frequently 
affected. 

Experimental investigations have shown that, under certain con- 
ditions, very similar appearances may be produced in the muscles by 
post-mortem changes. It is not unlikely that a variety of changes 
are at present included under the name waxy or hyalin degeneration 
of the muscles. 1 

Hypertrophy of Muscle. — True hypertrophy of muscle as a 
pathological condition is rare, but it has been described in a few 




Fig. 365.— Hyalin Degeneration (so-called Waxy Degeneration) op Abdominal Muscle in 

Typhoid Fever. 

cases. It is usually confined to circumscribed groups of muscles. 
On microscopical examination the diameter of the fibres is increased, 
sometimes considerably, though not uniformly. The transverse stri- 
ation is unaltered and the muscle nuclei are in some cases enlarged. 
The cause of the change is unknown. 

TUMORS. 

The tumors of the muscles usually develop in the connective 
tissue. Fibroma, chondroma, lipoma, myxoma, sarcoma may 
occur as primary tumors. Carcinomata and sarcomata may occur 
secondarily in the muscles as a result of local extension from adjacent 
parts. The muscle fibres are, as a rule, only secondarily affected by 
pressure, etc. , in tumors of the muscles, but there exist observations 



1 Consult Zenker, ' ' Ueber die Veranderung der willkurlichen Muskeln in Typhus 
abdominalis," Leipzig, 1864; also Weihl, "Exp. Unters. il. d. wachsartige Degene- 
ration der quergestr. Muskeln," Virch. Arch., Bd. lxi., p. 253, 1874. 






788 MUSCLE. 

which point to the possibility of a proliferation of the muscle nuclei 
and the new formation from them of cells which may take part in 
the growth of the tumor. 

PARASITES. 

The Trichina spiralis is the most common parasite in the mus- 
cles. 

Cysticercus cellulosoe and Echinococcus occasionally occur. 



PART IV. 



THE LESIONS FOUND 



IN 



THE GENERAL DISEASES, 



IN 



POISONING, 



AND IN 



VIOLENT DEATHS. 



62 



DISEASES OHAEACTEEIZED BY ALTEBA- 

TIO^S IN THE COMPOSITION OF 

THE BLOOD. 



There is a group of diseases in which the essential lesion seems to 
be an alteration in the composition of the blood, although in some 
members of the group other lesions are also present. This group 
embraces Chlorosis, Pernicious Anaemia, Addison's Disease, Leu- 
kaemia, and Pseudo-leukaemia. 

CHLOROSIS. 

Chlorosis is a disease of the blood attended with a diminution in 
the haemoglobin, and usually in the number of the red blood cells. 

Of the essential element in the causation of this disease and of the 
^xact method of its origin we are ignorant. The condition has been 
-attributed to congenital hypoplasia of the heart and blood vessels, to 
prolonged innutrition, to intestinal intoxication, and to functional 
disturbance of an unknown nature in the blood-producing organs. 

In the mildest grade of chlorosis the only change to be observed 
is a uniform diminution of haemoglobin. In severer forms may be 
added a diminution in number and moderate variations in size and 
shape of the red cells. In very severe and relapsing cases the hae- 
moglobin may be excessively decreased ; the red cells may number 
less than two million per centimetre; considerable alterations in size 
and shape of the red cells may occur; megalocytes, microcytes, and 
poikilocytes may appear, and the morphology of the blood as well 
as the clinical aspect of the disease may closely resemble or even 
become identical with progressive pernicious anaemia (see Plate, 
Fig. 2, page 80). 

The albuminous constituents of the plasma and the specific 
gravity of the blood are uniformly diminished, but the alkalinity and 
power of coagulation are slightly or not at all affected. Even in 
cases of considerable severity the degenerative changes in the viscera 
characterizing- other forms of anaemia have been found wanting, al- 
though degenerative changes in the red cells may occur in accordance 



792 DISEASES CHARACTERIZED BY ALTERATIONS 

with the severity of the disease. Haemoglobin is not set free in the 
plasma, the liver does not contain an excess of iron, and the urine 
is free from pathological urinary pigments. 

The regeneration of the blood in chlorosis under rest and treat- 
ment with iron may usually be rather promptly effected by increased 
activity probably accompanied by hyperplasia of the red marrow. 
This regenerative process may be indicated in the blood by the peri- 
odical appearance of considerable numbers of normoblasts. The 
appearance of these nucleated red cells may be accompanied by a 
moderate increase of leucocytes, both mononuclear and polynuclear, 
constituting the mixed leucocytosis characteristic of primary chlo- 
rosis. Myelocytes also may rarely be seen. 

PERNICIOUS ANEMIA. 

Pernicious anaemia is a disease of the blood and blood-forming 
organs, characterized by excessive destruction associated with defec- 
tive production of red cells. 

The exact relation of the factors concerned in the causation of the 
disease has not been determined. It may be said, however, that while 
very rapid cases of pernicious anaemia have been observed unaccom- 
panied by the usual lesions in the bone marrow causing defective 
haematogenesis, the disease seems not to exist without excessive hae- 
matolysis. 

Pernicious anaemia may probably originate as a primary disease 
of the blood or bone marroW, but many cases apparently idiopathic 
have been shown at autopsy to be secondary to such conditions as 
cancer, nephritis, tuberculosis, atrophy of the gastric mucosa, or the 
presence of parasites in the blood or intestine. The studies of Hunter 
indicate that the destruction of the blood may in some cases result 
principally in the portal circulation and particular^ in the spleen 
from the action of toxic principles absorbed from the intestines. 
Whatever its origin, the distinguishing feature of pernicious anaemia 
is the fact that the anaemia is entirely disproportionate to any appar- 
ent cause, and when once established tends to progress to a fatal issue. 

The essential lesion is an extreme and progressive diminution in 
number and very great variation in size and form of the red blood cells 
(see Plate, Figs. 3 and 4, page 80). Nearly constant is a general 
lesion of the bone marrow in which the normal nucleated red cells are 
replaced by an excessive number of larger nucleated corpuscles with 
hyperaemia and atrophy of fat cells. There is thus established an ab- 
normal type of development of red cells which closely resembles the 
. embryonal type. The destruction of haemoglobin is followed by a 
considerable deposit of iron in the liver, spleen, marrow, and other 



IN THE COMPOSITION OF THE BLOOD. 793 

organs, by the appearance of abnormal pigments in the urine, and by 
a yellowish discolorization of the skin. The prolonged anaemia may 
cause fatty degeneration of the viscera, especially of the liver, kidneys, 
and heart muscle. As a combined result of fatty changes in the 
arterial walls and of the diminution in albuminous principles and 
coagulability of the blood, haemorrhages in various parts of the body 
are of frequent occurrence. Disseminated areas of sclerosis in the 
spinal cord have been described and regarded as the result of minute 
haemorrhages in this region. 

In the blood the red cells are usually reduced to less than two 
million and often to half a million per cubic millimetre. Of the 
remaining cells a considerable percentage or nearly all may be ab- 
normally large (megalocy tes) . On the other hand, in a certain type 
of the disease many of the red cells are very small (microcytes). 
Cells of very irregular shape are often present in abundance (poiki- 
locytes). The quantity of haemoglobin in the majority of the cells is 
either increased as in one distinct type of the disease, or diminished 
as in other cases in which the individual cells may resemble those of 
chlorosis. The " haemoglobin index " — that is, the relation of the 
total percentage of haemoglobin to the total number of cells — may 
be normal when a deficiency of haemoglobin in one cell is counter- 
balanced by a proportionate excess in another. 

A variety of degenerative changes in the red cells are commonly 
present, including especially the change from haemoglobin to methae- 
moglobin, as indicated in those cells which stain reddish-brown with 
eosin. 

Nucleated red cells of normal size (normoblasts) are of rather in- 
frequent occurrence in the blood of well-established pernicious anae- 
mia. Abnormally large nucleated red cells (megaloblasts) are a 
nearly constant element and of great diagnostic importance, as they 
indicate the presence of a grave lesion in the bone marrow. 

Megalocytes and megaloblasts usually show an excess of haemo- 
globin, may exhibit amoeboid movement, and have no tendency toward 
the formation of rouleaux. Extremely large nucleated red cells 
(gigantoblasts) are frequently found in advanced cases, and in these 
cells as well as in the megaloblasts the nuclei may be seen in various 
stages of normal or pathological mitosis, while in their protoplasm 
may occasionally be demonstrated small basophile granules. In very 
rapid cases of pernicious anaemia both normoblasts and megaloblasts 
may be absent from the blood, in which event the yellow marrow of 
the long bones is not replaced by normal or pathological red marrow. 
During the rapid destruction of red cells haemoglobin may be dis- 
solved in the plasma, which in dry preparations stained with eosin 
takes on a reddish tinge. 



794 DISEASES CHARACTERIZED BY ALTERATIONS 

In the absence of complications producing leucocytosis, in perni- 
cious anaemia the leucocytes are usually diminished in number. Of 
the remaining white cells the mononuclear cells may be most abun- 
dant and a few myelocytes may be found. 

LEUKEMIA (LEUCOCYTH^EMIA)-. 

Leukaemia is characterized by a progressive increase of the white 
cells and decrease of the red cells of the blood, and by alterations of 
varying extent in the spleen, lymph nodes, and bone marrow. Leu- 
kaemia is probably to be regarded as a primary disease of the blood- 
forming organs. Many authorities, however, consider a change in 
the blood plasma to be the primary cause, and others, influenced by 
the discovery of bacteria in the blood of a few cases, believe in the 
infectious nature of the malady. The increase of uric acid in the 
blood and urine of leukaemia is thought by many to be of etiological 
importance. A close relation between leukaemia and some other 
diseases of the blood is indicated by the occasional undoubted devel- 
opment of leukaemia during the course of pernicious anaemia or 
pseudo-leukaemia. 

According to the predominance of the changes in one or other of 
the organs, various types of the affection may be distinguished. 
Myelogenous leukaemia indicates a special involvement of the bone 
marrow, but a pure form of this variety is extremely rare. Spleno- 
myelogenous leukcemia with changes in the spleen and marrow is 
more commonly seen. Lymphatic leukcemia, with alterations promi- 
nent in the lymph nodes, absent or inconsiderable in the spleen or 
marrow, is a common variety. Usually all three organs are simul- 
taneously involved. As a rule, other internal organs, liver, kid- 
neys, lungs, etc., show an infiltration of their capillaries with leu- 
cocytes, or the presence of numerous small collections of spheroidal 
cells. 

The lymphatic tissue in the gastro-intestinal tract and of other 
regions may be in a condition of hyperplasia. The changes referable 
to diminution of red cells and prolonged anaemia are similar to, but 
less pronounced than, those of pernicious anaemia. 

Ecchymoses in the serous and mucous membranes, or severe hae- 
morrhages on slight provocation, and fatty degeneration of the heart 
and kidneys, are frequent complications. Aside from various other 
foreign chemical substances which may exist in the blood in leukae- 
mia, there are very frequently found in the blood, marrow, spleen, 
liver, etc., after death elongated octahedral crystals, called Charcot's 
crystals, which are believed to be formed by a combination of phos- 
phoric acid with some organic base. 



IN THE COMPOSITION OF THE BLOOD. 795 

For a detailed description of the lesions of the different parts of 
the body in leukaemia, see chapters on Blood, Spleen, Lymph Nodes, 
Bones 5 etc. 

The specific gravity, alkalinity, and coagulability of the blood 
are uniformly diminished in leukaemia, as in other forms of progres- 
sive anaemia, but the morphology of the blood varies with the type of 
the disease and the predominance of the lesion in different organs. 
Aside from the rare conditions when, under proper treatment, the 
number of colorless cells may approach the normal, or when the 
toxaemia of an infectious disease replaces the mixed leucocytosis by 
the ordinary polynuclear leucocytosis, leukaemic blood always con- 
tains an excessive number of leucocytes (see Plate, Figs. 5 and 6, 
page 80). The colorless cells may even outnumber the red, but often 
more characteristic than the increase in numbers is the abnormal 
proportion of mononuclear cells and the abundance of myelocytes. 
In splenic and lymphatic leukaemia the increase is in the small and 
large mononuclear leucocytes. The presence of myelocytes in con- 
siderable numbers is a very constant feature of leukaemic blood and 
is believed to indicate the hyperaemia or further involvement of the 
bone marrow. Although found in moderate numbers in many other 
conditions, a considerable percentage of myelocytes is important 
diagnostic evidence of leukaemia. In nearly pure lymphatic leu- 
kaemia, large mononuclear and polynuclear leucocytes, myelocytes, 
and nucleated red cells may be comparatively infrequent, while the 
lymphocytes are greatly increased. 

The chronic process in the blood-producing organs, and the gen- 
eral disturbance of nutrition, may be indicated by an increase of 
eosinophile cells which is frequently observed, least often in the lym- 
phatic type of the disease. 

Mast cells are very constantly found in leukaemic blood, and the 
great rarity of their occurrence in other conditions renders their 
identification in the blood a valuable diagnostic sign. 

The leucocytes of leukaemia commonly show a diminution or 
absence of amoeboid motion. In the nuclei of myelocytes mitotic 
figures may be seen ; more frequently the nuclei show a deficiency of 
chromatin. In dry preparations from the blood of advanced cases, 
large, basket-shaped, faintly staining nuclei, apparently devoid of 
protoplasm, are frequently encountered (Plate, Fig. 5, page 80). 
Fatty degeneration of the protoplasm of leucocytes has been demon- 
strated, both in the circulation and in the bone marrow, and an 
increase cohesiveness may frequently be noted. 

The red blood cells in leukaemia exhibit, in a lesser degree, many 
of the changes characteristic of pernicious anaemia. In the lym- 
phatic type, normoblasts and megaloblasts may be very infrequent, 



796 DISEASES CHARACTERIZED BY ALTERATIONS 

but with the involvement of the marrow, especially in children, they 
may appear in considerable numbers. 1 



PSEUEO-LEUKJEMIA ("HODGKIN'S DISEASE," "ADENIE"). 

Under this term it has been customary to describe a rather hetero- 
geneous group of cases characterized by progressive anaemia, by 
hyperplasia of the lymph nodes and nodules, with an occasional but 
by no means constant involvement of the spleen, liver, and bone 
marrow, and by new growths of lymphatic tissues in many parts of 
the body. While anaemia of moderate or severe grade is very con- 
stantly present in this disease, the increase of leucocytes characteris- 
tic of leukaemia is wanting. 

Of the exact nature of the disease (if it be a single disease) very 
little is definitely known. The enlargement of the lymph nodes is in 
typical cases due to simple hyperplasia. The blood changes may 
present the type of pernicious anaemia, and in well-authenticated 
cases the condition has developed into true leukaemia. Recent evi- 
dence favors the belief that some cases classed under this heading 
may be of an infectious character. 2 Cases of primary sarcoma of 
the lymph nodes have been described as cases of pseudo -leukaemia. 

The condition found at autopsy varies greatly according to the 
distribution and character of the new growths of lymphatic tissue. 
The Emphatic nodules involved may be principally limited to the 
subcutaneous connective tissue (dermal type). Or the lymph nodes 
of the pharynx and neck may be chiefly involved (tonsillar type). 
Or the axillary or inguinal or mediastinal or retroperitoneal groups 
may be involved. A somewhat characteristic condition is produced 
by hyperplasia, often followed by ulceration, of the lymph nodules of 
the gastro-intestinal tract (intestinal type) . The hyperplastic lymph 
nodes may be isolated or they may be joined to form large lobulated 
masses. The enlarged lymph nodules may in the intestine project 
far into the lumen in spheroidal or polypoid form, and are sometimes 
dark in color as the result of the decomposition of haemoglobin of 
extravasated blood in the congested mucous membrane covering the 
nodules. Hyperplasia of the thymus has been described in associa- 
tion with the lesions of the lymph nodes. 3 A distinct sub-variety is 
that which terminates in leukaemia. In general any of the lymph- 
nodes or collections of lymphoid tissue may be involved, and nearly 

1 For further data with bibliography consult Midler, Central, f. allg. Pathol., 
v., 1894. 

2 Flexner, "Multiple Lympho-sarcomata, " Johns Hopkins Hospital Reports, vol. 
iii., p. 153. 

3 Brig idio and Piccoli, Ziegler's Beitr. z. path. Anat., Bd. xvi., p. 388. 



IN THE COMPOSITION OF THE BLOOD. 797 

every region has been a site of origin for the new growths of lym- 
phoid tissue, so that a great variety of combinations may be seen. 

The leucocytes in the blood may be slightly increased or dimin- 
ished, and in either case the mononuclear forms are usually in excess. 
Myelocytes have been observed in moderate percentage, but never in 
such proportions as in leukaemia. 1 

Ancemia infantum pseud o-leukcemica (von Jaksch) is a some- 
what peculiar form of anaemia occurring in children, and character- 
ized by progressive anaemia, by a considerable increase of leucocytes, 
by enlargement of the spleen and liver, and often by hyperplasia of 
the lymph nodes. 

By some authorities it is regarded as an early stage of leukaemia, 
by others as a form of secondary anaemia following rachitis, tuber- 
culosis, or syphilis. 

The histological changes in the blood-forming organs are, so far as 
is known, very similar to, but less pronounced than those of leukaemia. 
The enlargement of the spleen is usually greater than that of the 
liver, thus differing from infantile leukaemia, in which the liver and 
spleen are equally affected — while the involvement of the lymph nodes 
is less frequent than in leukaemia. 

The red cells present most of the changes of pernicious anaemia, 
but nucleated red cells are often found in great abundance. The leu- 
cocytes ma}' number one hundred thousand per cubic millimetre, the 
increase affecting the mononuclear cells chiefly, the eosinophile cells 
slightly, and of both a considerable percentage may be myelocytes. 

1 Consult Monte and Berggrun, "Die chronische Anaemie d. Kindesalter, " Leipsic, 
1892. 






SOORBUTUS-PURPUEA-H^EMATOPHILIA. 



SCORBUTUS (SCURVY) 



This disease appears to result from imperfect nutrition under 
conditions which cannot be considered here, and whose immediate 
cause we do not understand. The lesions are variable, the most 
prominent being anaemia; extravasation of blood in the skin, subcu- 
taneous tissue, and muscles; swelling and ulceration of the gums. 
Small and sometimes extensive haemorrhages are apt to occur in the 
mucous membranes and on serous surfaces. Small ulcers may form 
in the mucous membranes. Fatty degeneration of the heart, liver, 
and kidneys is not uncommon. The spleen may be large and soft. 
No constant characteristic changes have been discovered, either in 
the blood vessels or the blood, which would satisfactorily account for 
the extravasations and other lesions. 

The body is apt to decompose early. The skin may be mottled 
with small and large purple, blue, brown, or blackish spots produced 
by degenerative changes in the extravasated blood in the cutis. 
Sometimes ulcers are produced by the perforation of effused blood on 
to the surface. 

The joints may be inflamed, may contain serum or blood. Rarely 
the haemorrhages are followed by destruction of the cartilages and 
ends of the bones. 

Very rarely there is haemorrhage between the periosteum and 
bone, and in the bone itself, producing softening and destruction of 
the bone, and separation of the epiphyses. The sternal ends of the 
ribs are the most frequent seat of this change. 

That some forms or phases of scorbutus are of infectious nature 
is not improbable, but definite data in this direction are wanting. 1 

PURPURA HEMORRHAGICA (MORBUS MACULOSUS) . 

This disease is characterized by the occurrence of ecchymoses in 
the skin, mucous and serous membranes. Haemorrhages, particu- 

1 For a study of scorbutus in infants consult Northrup and Crandall, New York 
Med. Jour., May 26th, 1894. 



SCORBUTUS — PURPURA — H^MATOPHILIA. 799 

larly from the mucous membranes, may be very severe and even 
fatal. The cause of the disease is unknown. A few cases have been 
described under this name in which the characteristic ecchymoses 
were associated with the pyogenic bacteria, representing, it would 
seem, a phase of pyaemia. Whether any considerable number of 
cases of this disease are associated with bacteria we do not yet 
know. 1 

HJEMATOPHILIA (HEMORRHAGIC DIATHESIS). 

This abnormal condition consists in a liability to persistent hae- 
morrhage on the slightest provocation, and is dependent upon some 
constitutional peculiarity which is unknown to us. It is frequently 
hereditar}'. An unusual thinness of the intima of the arteries has 
been noticed in some cases, and other changes have been described ; 
but there are no constant lesions associated with haemorrhages, as yet 
discovered, which would satisfactorily explain their occurrence. The 
haemorrhages may be traumatic in origin, or they may occur sponta- 
neously from the mucous membranes. 

1 For a more detailed consideration in the light of recent studies of cases often 
grouped under the name " Hemorrhagic Infections, " consult Honl, Ergebnisse der 
allg. Aetiologie, 1896, p. 793 (bibliography). 



ADDISON'S DISEASE. 



This name is applied to a disease especially characterized by a 
peculiar pigmentation of the skin and by certain changes in the ad- 
renals. The patients become very ansemic, but are not emaciated. 
They suffer from cerebral symptoms, great prostration, syncope, and 
derangements of the functions of the stomach and intestines. 

The pigmentation of the skin is the symptom which has especiall}- 
attacted attention. The change in color usually begins and becomes 
most marked in those parts of the skin which are not covered by the 
clothing or are naturally darker colored. The rest of the skin after- 
ward changes color, but not uniformly, white patches being left. 
The color is at first a light yellow or brown ; this becomes darker un- 
til it is of a dark greenish, grayish, or blackish brown. The mucous 
membrane of the tongue, lips, and gums may be pigmented in the 
same way. 

Under the name of Addison's disease different observers have de- 
scribed cases in which the symptoms and bronzed skin existed with- 
out disease of the adrenals; cases in which the bronzed skin was the 
only lesion; and cases in which the adrenals were diseased without 
symptoms or bronzed skin. 

We hardly know as yet what are really the characteristic lesions 
of the disease. 

The Skin. — The discoloration of the skin is due to deposit of yel- 
lowish-brown pigment in the deeper layers of the epidermis, espe- 
cially in the layer covering the papilke, and less constantly in the 
connective tissue of the cutis. 

The Brain. — Pigmentation of the gray matter, acute meningitis, 
chronic meningitis, and distention of the ventricles with serum have 
been observed. 

The Heart. — The muscular fibres ma} r be the seat of fatty degen- 
eration. 

The Sympathetic Nerves may show a variety of changes ap- 
parently due to chronic inflammation, especially the nerves which 
are in contact with the adrenals. Various changes in the semilunar 
ganglia have been described. 



ADDISON'S DISEASE. 801 

The Adrenals. — The most common lesion of these bodies is a 
tuberculous inflammation, and this or some other lesion of the ad- 
renals has been found in nearly one-half of the cases. On the other 
hand, it should be remembered that similar lesions of the adrenals 
often occur without other indications of Addison's disease. 

Tuberculous adrenals may be large, hard, and nodular; less fre- 
quently of normal size or smaller than normal. On section they may 
contain cheesy masses surrounded .by zones of gray, semi-translucent 
tissue. Later the cheesy masses may become calcified or they may 
soften and break down. The grayish zones are composed of tubercle 
tissue, or denser connective tissue. 

Other cases have been described in which the adrenals were the 
seat of carcinoma or of fatty or waxy degeneration. The adrenals in 
some cases appear normal or they may be atrophied. 

On the whole the clinical, morphological, and experimental data 
now available seem to point to both the sympathetic system and to 
the adrenals as of greatest significance in determining this disease. 
But exact knowledge in the matter depends upon a much more defi- 
nite understanding than is now possible of the functions and rela- 
tionship of the adrenals and the nervous system. 1 

1 For a summary of the available observations on Addison's disease up to 1893 
consult Thompson, Trans. Assn. Am. Phys., vol. viii., p. 34. Consult also v. 
KaMden, Ziegler's Beitr. z. path. Anat., Bd. x., p. 494. On»the relationship of 
the suprarenal bodies to the nervous system, consult Alexander, ibid., Bd. xi., 
p. 145. For observations on the effects of removal of suprarenal body see Tizzoni, 
ibid., Bd. vi. For recent and general bibliography consult Lubarsch, Ergebnisse d. 
spec. path. Morphologie u. Physiologie, 1896, p. 488. 



GOUT. 



The characteristic lesion of gout is the presence of an abnormal 
amount of uric acid in the blood and the deposit of urate of soda in 
the articular cartilages, the ligaments of the joints, the ears, and the 
eyelids. 

The most frequent situation is the metatarso-phalangeal joint of 
the great toe. The cartilage may be infiltrated or encrusted with 
the deposit. 

A very important feature of gout is that patients with the gouty 
diathesis are especially liable to derangements of digestion and to 
certain chronic inflammations, such as chronic inflammation of the 
arteries, chronic bronchitis, and chronic nephritis. 



ACUTE KHEUMATISM, 



There are no characteristic lesions in this disease, which in many 
respects resembles the infectious maladies. It is apt to be associated 
with inflammation, with little exudate in various joints, and with 
inflammation of the heart or pericardium. In cases in which sup- 
purative inflammation has occurred, pyogenic bacteria have been 
occasionally found. But the cause of the disease itself is unknown. 



DIABETES MELLITUS. 









There are no constant or characteristic morphological lesions of 
this disease, which involves such defects in nutrition as lead to an 
abnormal accumulation of sugar in the blood and its discharge by 
the urine. 

A great variety of lesions have been found in the body after death 
from diabetes, but none of them and no combination of them appear 
to be of well-defined significance in this special relationship. 

The Brain may appear to be entirely normal; it may be con- 
gested ; there may be an increase of serum ; the convolutions may be 
shrunken; there may be meningitis; there may be dilatation of the 
blood vessels, small extravasations of blood around the vessels, en- 
largement of the perivascular spaces, and alterations in the perivas- 
cular sheaths and nerve tissue bounding the cavities; there may 
be tumors at the base of the brain. 

The Spinal Cord may present dilatation of the blood vessels; 
dilatation of the central canal ; changes in the gray matter of the an- 
terior cornua. 

The Lungs. — There may be pleurisy, bronchitis, broncho-pneu- 
monia, lobar pneumonia, gangrene of the lung, chronic pulmonary 
phthisis. 

The Heart is often small; there may be chronic endocarditis. 

The Stomach and Intestines. — The stomach may be dilated, its 
walls may be thickened, there may be hsemorrhagic erosions of the 
mucous membrane. In the intestines there may be tuberculous ulcers 
or enteritis. 

The Liver may be cirrhotic or fatty. 

The Kidneys may be enlarged ; they may be the seat of paren- 
chymatous degeneration or diffuse nephritis; there may be glycogenic 
degeneration of the epithelium of Henle's loops. 

The Blood. — In a few cases fat has been found in the blood, and 
fat emboli in the vessels of the 1 Lings. 

Attention has, however, been called to the pancreas, which in a 
considerable proportion of cases may show atrophy of the parenchyma 






DIABETES MELLITUS. 805 

with increase of the interstitial tissue or other lesions. Similar le- 
sions of the pancreas may, however, occur without the existence of 
diabetes. The results of partial or total extirpation of the pancreas 
lend weight to the importance of this organ in the etiology of dia- 
betes. 1 

1 Reference to the more important work on this subject may be found in an 
article by Ka&ahara, Yirch. Arch., Bd. cxliii., p. Ill, 1896. 
63 



SUNSTEOKE (INSOLATION). 



During the hot summer months cases of sunstroke are of frequent 
occurrence in New York. The persons affected are, for the most 
part, adult male laborers, usually of intemperate habits. 

It is necessary to separate from the cases of sunstroke proper, 
when the patient is attacked while exposed to the heat of the sun, 
the cases of exhaustion from heat and fatigue, which may occur as 
well in the house. 

The patients who are seriously affected by sunstroke exhibit, dur- 
ing life, an intense heat of the skin, convulsions, and coma. Death 
in many cases soon ensues. In other cases the symptoms are more 
protracted. 

After death, decomposition sets in very early, owing to the state 
of the weather. In autopsies which we have made within two hours 
after death the increased heat of the skin was still maintained. 

The Brain and its membranes were in some cases congested, in 
others not. Sometimes there was an increased amount of serum be- 
neath the pia mater ; sometimes there were small and thin extrava- 
sations of blood beneath the pia mater and between the pia and dura 
mater. 

In the other viscera there were no lesions except those due to the 
condition of coma existing before death. The lungs and kidneys 
were frequently congested. 

In the cases in which cerebral symptoms are protracted for a num- 
ber of days the lesions of meningitis have been found after death. 

Attention has been called by Dr. H. C. Wood, Jr., to the rigid 
condition of the wall of the heart after death, but this rigidity is cer- 
tainly not present in all cases. 

According to Cramer, 1 persons surviving for some time the first 
severe effects of the heat may suffer important alterations in certain 
nerve fibres of the brain. 

1 Cramer, Centralblatt fur allg. Path., etc., March 15th, 1890. 



DEATH FEOM BTJENIN"G. 



Death may be caused by the inspiration of smoke and flame ; by 
drinking of hot fluids ; by the direct contact of flame or hot sub- 
stances with the external surface of body. It may be due to the di- 
rect effect of the agents, to secondary affections of the viscera, or to 
the exhaustion produced by long-continued inflammation and sup- 
puration. 

Sudden death may occur after extensive burnings of the skin. ' 

The entire body may be burned to a coal or completely roasted, or 
only a larger or smaller area of the skin be burned. 

We find the burned skin divested of epidermis and presenting a 
peculiar red, hard, parchment-like appearance. If the patient has 
lived some time, this is replaced by a suppurating surface. Or there 
are small, bladder-like elevations of the epidermis. The base of 
these blisters is red and they are surrounded by a red zone, or sup- 
puration may have commenced. 

These appearances cannot be produced by heat applied to the 
skin after death. 

The Brain may be congested, cedematous, or softened. More 
frequently it is normal. 

The Larynx and Trachea may be congested and the seat of 
croupous inflammation. There may be oedema of the glottis. 

The Lungs may be congested and cedematous, or hepatized, or 
the seat of pysemic infarctions. There may be pleurisy. 

Inflammation of the peritoneum is not very infrequent. There 
may be swelling of the solitary and agminated nodules of the small 
intestine. 

The duodenum may be the seat of perforating ulcers, and the mu- 
cous membrane of the entire gastro-intestinal canal may be con- 
gested. The Liver, Spleen, and Kidneys may be the seat of pa- 
renchymatous degeneration or of p3 r aemic infarctions. 

1 For literature on sudden death following severe burns consult Silbermann, 
Virch. Arch., Bd. cxix., p. 488, 1890. 



DEATH FROM ELECTRICITY. 



Lightning. — Persons who are struck by lightning may die in- 
stantly ; or may continue for several hours comatose or delirious, and 
then either die or recover ; or they may die after some time from the 
effects of the burns and injuries received. 

The post-mortem appearances are very variable. Sometimes 
there are no marks of external violence or internal lesions. Some- 
times the clothes are burnt and torn, while the skin beneath them is 
unchanged. Usually there are marks of contusion and laceration, or 
ecchymoses, or lacerated, punctured wounds, or fractures of the bones, 
or superficial or deep burns. The track of the electric fluid may 
sometimes be marked by dark-red arborescent streaks on the skin. 
Fractures are rare. 

The internal viscera may be lacerated and disorganized from 
lightning. 

Artificial Electrical Currents. — In death from powerful artifi- 
cial electrical currents, either by accident, as in linemen and others, 
or in electrical executions, there may be local burnings of varying 
degree where the wires or electrodes come in contact with the skin. 
The clothes may be pierced with holes at the point of exit of the 
current. 

Internally there appear to be no marked or characteristic lesions, 
either gross or microscopical, in this form of death. 

Van Gieson 1 and others have observed the occasional, but not 
constant, occurrence of small haemorrhages in the floor of the fourth 
ventricle, the significance of which is doubtful. Other petechial 
spots have been observed beneath the serous surfaces of the endo- 
cardium, pericardium, and pleura, and on the spleen. 

1 Van Gieson, "A Report of the Gross and Microscopical Examination of Six 
Cases of Death by Strong Electrical Currents." Reprint from the New York Medi- 
cal Journal, May 7th and 14th, 1892. 



DEATH FROM SUFFOCATION- ASPHYXIA. 



By suffocation we understand that condition in which air is pre- 
vented from penetrating into the lungs without direct pressure on 
the larynx or trachea. The interruption of the function of respira- 
tion which is thus brought about induces the condition known as 
asphyxia. Many deaths from drowning and strangulation take 
place in this way. 

The methods in which the supply of air may be cut off from the 
lungs are very various. The mouth and nose may be closed by the 
hand, by plasters and cloths, by wrapping up the head in cloths, by 
covering the face with earth, hay, grain, etc. Foreign bodies may 
be introduced into the mouth, pharynx, and larynx. Blood may 
pass into the trachea from an aneurism or from a wound. The glot- 
tis may be closed by inflammatory swelling. Matters which are 
vomited may lodge in the larynx. 

On the other hand, injury or disease of the medulla oblongata, or 
paralysis or spasm of the muscles of respiration from drugs, tumors 
pressing upon the air passages, or diseases of the lungs themselves, 
may induce asphyxia. 

EXTERNAL INSPECTION. 

The body should be examined for marks of violence, the cavities 
of the mouth and nose for foreign substances. 

The face maybe livid and swollen or present a natural appear- 
ance. The conjunctiva may be congested and ecchymotic. There 
may be small ecchymoses on the face, neck, and chest. The mouth 
often contains frothy blood and mucus. The tongue may be pro- 
truded. 

INTERNAL EXAMINATION. 

The Brain and its membranes may be congested, or anaemic and 
^edematous, or unchanged. 

The Blood throughout the body is unusually dark-colored and 
fluid. 



^ 



I 



810 DEATH FROM SUFFOCATION — ASPHYXIA. 

The Larynx may contain foreign bodies which have produced the 
suffocation. The mucous membrane of the larynx, trachea, and 
bronchi is congested and sometimes ecchymotic. These passages 
contain frothy blood and mucus. 

The Lungs are usually congested and ©edematous, but sometimes 
do not differ from their ordinary appearance. There may be small 
patches of emphysema near the surface of the lungs. Sometimes, 
especially in infants, small ecchymoses are found in the costal and 
pulmonary pleura. 

The Heart usually presents its right cavities full of blood, its, 
left cavities empty ; but to this there are frequent exceptions. 

The Abdominal Viscera are usually congested. 

DEATH FROM STRANGULATION— HANGING. 

Strangulation is effected by the weight of the body in hanging, 
by pressure on the neck with the hands or by some other object, or 
by constriction of the neck with a cord or ligature of some kind. 
Death is usually produced by asphyxia, or by asphyxia combined 
with the effect of the cutting-off of the blood supply to the brain by 
pressure on the large vessels of the neck. In some cases of hanging, 
death ensues as a result of fracture or dislocation of the cervical ver- 
tebrae. 

EXTERNAL INSPECTION. 

The face may be livid and swollen, the eyes prominent, the lips 
swollen, and the tongue protruded. These appearances are, how- 
ever, often absent. Erection of the penis, BJaculation of semen, and 
evacuation of faeces and urine are frequently observed. 

In most cases marks are left upon the neck by the objects which 
have directly produced the strangulation. 

In cases of hanging, the mark about the neck varies considerably 
in position, direction, and general characters, depending upon the 
kind of ligature employed, the time of suspension, period after death 
at which the observation is made, etc. The most common mark 
left by a cord about the neck is a dry, dense, brownish furrow, 
whose breadth corresponds but in a very general way with the 
diameter of the cord. In some cases, according to Tidy and others, 
there may be no mark at all if the hanging is quickly accomplished 
with a soft ligature and the body cut down immediately after death. 
There may be abrasions and ecchymoses of the skin at the seat of 
ligature. 

In cases of strangulation by the fingers the marks on the neck 
may correspond in a general way to the shape of the fingers. 



DEATH FROM SUFFOCATION — ASPHYXIA. 811 

The application of the same forces immediately after death may 
produce the same marks as when death is induced by them. 

INTERNAL EXAMINATION. 

The Brain and its membranes may be congested, or there may 
be extravasation of blood, or there maybe no abnormal appearances. 

The Neck. — In some cases there is effusion of blood beneath the 
ligature, rupture of the cervical muscles, fracture of the os hyoides 
and cartilages of the larynx, fracture and dislocation of the cervical 
vertebrae, rupture of the internal vertebral ligaments and of the inner 
and middle coats of the carotid arteries. Similar changes may be 
produced in the dead body by the use of great violence. In death 
from asphyxia the lesions are similar to those described above. In 
some cases — for example, where death has occurred from fright or 
shock — the results of post-mortem examination are entirely negative. 

DEATH FROM DROWNING. 

In examining the bodies of persons who have been drowned it is 
necessary to bear in mind a number of questions which may arise : 
Whether the person came into the water alive or dead ? How long 
a time has elapsed since death ? Whether the person committed sui- 
cide, or was drowned by accident, or was murdered ? These ques- 
tions are to be solved sometimes certainly, sometimes with proba- 
bility, sometimes not at all, by the post-mortem examination. 
Persons dying in the water, to which condition the term drowning 
is commonly applied, may die from asphyxia, from exhaustion, from 
fright or syncope, from diseases of the heart, apoplexy, injuries, etc. 
While in the majority of cases asphyxia is a predominant or impor- 
tant factor in death by drowning, the conditions under which death 
occurs are so apt to be complex that in the minority of cases only are 
the lesions of pure asphyxia found after death, while in most cases 
the bodies present the more or less well-marked lesions of asphyxia 
together with those indicative of complicating conditions. There are 
no post-mortem conditions which alone are absolutely characteristic 
of drowning, and it is only by considering all the facts elicited by 
the autopsy together that any just conclusion can be arrived at. It 
should always be borne in mind, moreover, that even the most char- 
acteristic of the evidences of drowning are apt to be modified or to 
disappear as decomposition goes on. 

EXTERNAL INSPECTION. 

Post-mortem rigidity usually sets in early, sometimes immediately 
after death. Decomposition goes on, especially in summer, with 



812 DEATH FROM SUFFOCATION — ASPHYXIA. 

unusual rapidity in bodies which have been removed from the water. 
Frequently, but by no means constantly, the peculiar roughening of 
the skin, known as goose skin (cutis anserina), is found, but this may 
occur after death from other causes. A light, lathery froth, either 
white or blood-stained, is frequently seen about the mouth and nos- 
trils within twelve to twenty -four hours after removal of the body 
from the water, but it may be absent, and may be seen after death 
from other causes. After the body has lain for several hours in the 
water (twelve to twenty -four) the thick skin of the palms of the 
hands and soles of the feet may become macerated and thrown into 
coarse wrinkles, just as it may after prolonged soaking during life, 
or in a dead body thrown into the water. The penis and nipples 
may be retracted and the scrotum shrunken, but this is not constant 
nor characteristic. 

If the person has struggled in the water and clutched at objects 
within his reach, there may be evidences of this in excoriations of 
the fingers or in the presence of sand, weeds, etc., under the nails or 
grasped in the hands. 

External marks of injury, bruises, etc., should be sought for, 
since persons in diving, or on being thrown into the water with homi- 
cidal intent, may have died from the violence, and not, strictly speak- 
ing, from drowning. It should also be borne in mind in such com- 
plex cases that injuries, not in themselves fatal, may, when the body 
is in the water, prove so on account of the inability of the person to 
rescue himself or gain time for recovery from the injury, and that 
then the struggle for breath may be but slight, and the more promi- 
nent signs of drowning but little marked. 

INTERNAL EXAMINATION. 

The Brain. — Congestion of the brain and its membranes is found 
only in a small proportion of cases. 

The Blood, when death occurs from asphyxia, is usually fluid 
throughout the body and of a dark color, as in asphyxia from other 
causes. 

The Air Passages.— In persons who die from asphyxia the mu- 
cous membrane of the larynx, trachea, and bronchi is usually con- 
gested, and the air passages contain a variable quantity of bloody or 
mucous froth. In persons dying in the water from other causes than 
asphyxia these appearances are absent. Foreign substances from the 
water, such as sand, weeds, etc., or matters regurgitated from the 
stomach, may find their way into the air passages during the act of 
drowning or as a post-mortem occurrence. Thus, in bodies washed 
about on the bottom, sand or mud may get into the air passages for 
a certain distance, from the mechanical action of the water. 



DEATH FROM SUFFOCATION — ASPHXIA. 813 

The Lungs in typical cases are distended so that they fill the 
thorax and cover the heart. The increased size is due partly to con- 
gestion, partly to the presence of the fluid in which the person was 
drowned, which is often inspired during the act of drowning, and 
partly to the distention of the air vesicles with air. While, in cases 
of drowning in which there is a struggle and water is breathed in, 
the lungs contain more or less fluid, this may, as a result of decom- 
position, find its way in greater oriess quantity into the pleural cavi- 
ties by transudation, leaving the lungs comparatively empty. It 
should be remembered, however, that a considerable quantity of 
reddish fluid may collect in the pleural cavities under other condi- 
tions than drowning, as a post-mortem change, by transudation from 
the blood vessels and other adjacent tissue. 

The Heart. — In those who die from asphyxia the right cavities 
are usually filled with fluid blood, while the left cavities are empty. 
But where death is due to complex causes this may not be the case. 

The Stomach. — The fluid in which the person was drowned, 
sometimes mixed with sand, weeds, etc., may be swallowed during 
the act of drowning. Sand may wash for a short distance into the 
oesophagus after death, in bodies washing about the bottom. 

The Abdominal Viscera may be congested in persons who die 
from asphyxia. 

In persons dying from syncope, shock, etc., we may find no 
lesions. When the death is partly due to asphyxia and partly to 
other causes, the conditions will vary in various ways, which need 
not be described in detail here. 

In important cases of doubtful drowning it is desirable to care- 
fully collect and save some of the fluid from the lungs and stomach 
for micro-chemical examination, since the identification of these 
fluids with those in which the person was presumably drowned will 
often give certainty to an otherwise doubtful case. 

For the detailed consideration of the anatomical diagnosis of 
drowning, the changes which bodies dead from drowning undergo 
from decomposition, and the factors bearing on the question of sui- 
cide, homicide, etc., we refer to works on medical jurisprudence. 1 

1 Tidy, "Legal Medicine," vol. ii , pp. 342-373. Guy and Ferrier, "Forensic 
Medicine," pp. 274-285. 



DEATH FROM POISONING. 



In cases of suspected poisoning which may possibly have a medi- 
co-legal bearing the examination should be made with extreme care 
and thoroughness. The inspection of the body and the examination 
of all the viscera should be thorough and detailed. Every appear- 
ance should be noted at the time and nothing left to the memory. 
It is well to have an assistant record the observations as they are 
made. The disposition of the parts and organs in jars should also 
be noted at the same time. 

It is important to remember that many poisons destroy life with- 
out producing appreciable lesions, and also that many cases of sud- 
den death occur, not due to poisons, and without any discoverable 
cause. 

In bodies which are exhumed for examination the tissues may be 
so changed by decomposition that it is impossible to say whether 
lesions have or have not existed. In such cases the careful and 
separate preservation of the viscera and other parts for chemical ex- 
amination is often all that can be done. For directions for preserving 
tissues and organs for the chemist in medico-legal cases, see Part I. 
(page 41). 

SULPHUEIC ACID. 

The effects of this poison vary with the amount taken and with 
its strength. Death usually takes place in from two to twenty-four 
hours after the taking of the concentrated acid. A case of death 
within an hour is recorded. When the poison is less concentrated 
or its effects less intense, the patient may survive for months. 

The skin of the face about the mouth may be blackened and 
charred by the acid. The mouth and pharynx are of a grayish or 
blackish color, or are covered with a whitish layer, while the deeper 
tissues are reddened. Sometimes these regions escape the action of 
the poison. 

The larynx, trachea, and lungs are sometimes acted on, softened 
and blackened by the accidental passage of the acid into them. 



DEATH FROM POISONING. 815 

This may even take place when the acid does not pass into the oeso- 
phagus. 

The oesophagus seldom escapes. It is grayish or blackish col- 
ored, softened, and the mucous membrane comes off in shreds. If 
life is prolonged, cicatrices and strictures are formed. The stomach 
may contain a blackish, pulpy fluid, due to the action of the acid on 
mucus, blood, etc. It is coated on its internal surface with a black, 
sticky layer, beneath which the mucous membrane is reddened. 
The mucous membrane may be blackened in patches or stripes. The 
organ may be contracted and the mucous membrane corrugated. 
Sometimes perforation takes place and the acid blackens and 
softens the adjoining viscera. In protracted cases cicatrices are 
formed and the organ is contracted. If the poison is dilute there 
may be only the lesions of chronic gastritis. 

The blood is sometimes thickened, syrupy, acid, and may form 
thrombi in the vessels. 

^The body may be partially preserved from decomposition, owing 
to the action of the acid upon the tissues. 

Fatty degeneration of the renal epithelium is mentioned by some 
authors. 

The solution of indigo in sulphuric acid, commonly known as 
sulphate of indigo, produces the same lesions as sulphuric acid, and 
also stains the tissues with which it comes in contact of a dark-blue 
color. It is stated that an indigo-blue tint is often found in the 
mucous membranes after poisoning by pure sulphuric acid. 1 

NITRIC ACID. 

Death may occur very soon after the taking of the poison, but 
does not usually occur for several hours, and may not take place for 
several days or weeks. 

The surface of the mucous membrane of the mouth, pharynx, 
and oesophagus is covered with yellow eschars wherever the acid has 
touched it. Beneath and around the eschars the tissues are con- 
gested and red. The poison may be introduced into the oesophagus 
without acting on the mouth. The stomach contains a viscous, 
sanguinolent, yellow or greenish fluid. The mucous membrane is 
congested, red, swollen and softened, ecchymotic. It is rarely per- 
forated. The duodenum may be inflamed, and the inflammation 
extend to its peritoneal coat. The rest of the intestines usually 
escapes the action of the acid. 

The larynx is very frequently acted on by the acid. There are 

1 Woodman and Tidy , "Forensic Medicine and Toxicology," ed. 1877, p. 237. 



816 DEATH FROM POISONING. 

yellow eschars, congestion and swelling of the mucous membrane, 
sometimes oedema of the glottis. The trachea may be inflamed and 
the lungs congested. 

If the patient survives the first effects of the poison the lesions of 
chronic inflammation, cicatrization, and contraction may be found 
at a later period. 

The acid nitrate of mercury, if taken in a concentrated form into 
the stomach, may produce the same lesions as nitric acid. 

HYDROCHLORIC ACID. 

In fatal cases death occurs on the average in about twenty-four 
hours. The lesions are in general similar to those produced by sul- 
phuric and nitric acids, except that the eschars are usually of a whit- 
ish color at first, becoming, after a time, discolored and disinte- 
grated. It is also more common to find false membranes on the in- 
flamed surfaces. 

OXALIC ACID. 

In fatal cases death may occur within ten minutes (in one case in 
three minutes) or may be delayed for two or three weeks. The pe- 
riod of death does not depend, as do in general the symptoms, upon 
the amount and concentration of the poison. 

The mucous membrane of the mouth, pharynx, and oesophagus 
is usually white and shrivelled, and easily peeled off, and may be 
covered with brownish vomit from the stomach. The oesophagus 
may be much contracted. The stomach is usually contracted and 
contains a dark-brown, acid, mucous fluid. The mucous membrane 
of the stomach may be pale, soft, and easily detached, sometimes 
looking as if it had been boiled in water. Sometimes it is red and 
congested ; sometimes blackened and gangrenous ; sometimes peeled 
off in patches. Perforation is of rare occurrence. If life be pro- 
longed the whitened condition of the mucous membrane is succeeded 
by congestion and inflammation. The small intestines may be in- 
flamed. Inflammation of the pleura and peritoneum, and conges- 
tion of the lungs, are of occasional occurrence. In some cases of 
death from oxalic acid there are no well-marked lesions. 

Potassium oxalate produces the same lesions as oxalic acid. 

TARTARIC ACID. 

This acid is seldom used as a poison, but in large doses may prove 
fatal. The lesions in the cases observed were redness and inflam- 
mation of the mucous membrane of the gastro-intestinal canal. 



DEATH FROM POISONING. 817 



POTASH, SODA, AND THEIR CARBONATES. 

These substances are not commonly used as poisons with suicidal 
or homicidal intent, but may be taken by mistake. They may cause 
death in a few hours, or life may be prolonged for several weeks. 

The mucous membrane of the mouth, pharynx, oesophagus, and 
stomach is softened, swollen, congested, and inflamed, or may be 
peeled off. It may be blackened from local changes in the blood. 
The mucous membrane of the larynx and trachea may also be swol- 
len and inflamed. . 

If life is prolonged for some time, cicatrices and strictures of the 
oesophagus and stomach are apt to be produced as a result of the 
reparative inflammation. 

AMMONIA. 

The vapor of strong ammonia may cause death from inflamma- 
tion of the larynx and air passages. The strong solution of am- 
monia produces lesions similar to those of potash and soda. The 
larynx, trachea, and bronchi are frequently inflamed, and may be 
covered with false membranes. Fatal inflammation of the rectum 
and colon has been produced by an enema of strong solution of am- 
monia. 

POTASSIUM NITRATE. 

Accidental poisoning sometimes occurs from large doses of this 
salt. In the observed cases there were intense congestion and in- 
flammation of the stomach and intestines, and in one case a small 
perforation of the stomach. 

For the effects of several infrequently employed salts of the alka- 
lies and alkaline earths, which for the most part produce simple in- 
flammation of the gastro-intestinal canal, we refer to special works 
on toxicology. 

PHOSPHORUS. 

Poisoning by phosphorus is much more common in France and 
Germany than in this country. Some of the forms of rat poison, of 
which this is a frequent ingredient, and the ends of matches, are 
common media for its administration. It is more often used with 
suicidal than homicidal intent. 

The post-mortem appearances vary according to the length of 
time which elapses before death, which may be from a few hours to 
several months. 

If death takes place in a few hours the only lesions may be those 
produced by the direct local action of the poison. The mouth, pha- 



818 DEATH FROM POISONING. 

rynx, and oesophagus usually escape. The stomach may be only 
slightly reddened, or there may be patches of inflammation and 
erosion. The contents of the stomach are often mixed with blood 
and may have the peculiar smell of phosphorus. There may be little 
bits of wood present when the poison has been taken from the heads 
of lucifer matches. It is said that the mucous membrane of the 
stomach may emit a phosphorescent light in the dark. 

If death does not ensue until after several days the lesions are 
more marked. The body is usually jaundiced. There may be ecchy- 
mosis beneath the pericardium, pleura, and peritoneum, in the lungs, 
the kidneys, the bladder, the uterus, the muscles, and the subcuta- 
neous connective tissue, and bloody fluid in the visceral cavities. 

The heart and voluntary muscles, the walls of the blood vessels, 
and the endothelium of the air vesicles of the lungs may be in the 
condition of fatty degeneration. The blood is usually dark and fluid. 

The stomach sometimes presents no very striking changes. There 
may be small circumscribed spots of inflammation, erosion, or gan- 
grene, and occasionally perforation. The most constant change is a 
granular degeneration of the cells which fill the gastric follicles. In 
consequence of this the mucous membrane appears thickened, opaque, 
of white, gray, or yellow color. 

The small intestine appears normal or is congested. 

The liver is found in different degrees of parenchymatous and 
fatty degeneration, and is often stained yellow from the jaundice. 
It is usually increased in size and of a grayish, grayish-yellow, or 
light-yellow color, unless stained by the bile. Less frequently the 
centres of the acini are congested, or the entire liver is congested, or 
there are small haemorrhages in the liver tissue. The liver may be 
soft, flabby, and smaller than normal. In the interstitial tissue of 
the liver and along the branches of the portal vein there may be 
marked infiltration with small spheroidal cells. 

The kidneys often present parenchymatous and fatty degenera- 
tion of the epithelium. The mesenteric lymph nodes may be soft 

and swollen. 

ARSENIC. 

This poison is very frequently employed with suicidal intent. 
Death may occur in a longer or shorter time from the direct irrita- 
tive effects of the poison upon the gastro-intestinal canal, with the 
symptoms which usually accompany the ingestion of irritant poisons ; 
or it may occur with symptoms of collapse, or coma, or shock ; or 
the symptoms may resemble those of cholera. The average time of 
death in acute fatal cases is about twenty hours, but death has 
occurred in twenty minutes and has been prolonged for two or three 
weeks. 



DEATH FROM POISONING. 819 

The mouth, pharynx, and oesophagus may be inflamed, but are 
more frequently unaltered. The stomach may be empty or contain 
mucus mixed with blood. The arsenic, in substance, may be found 
adherent to the mucous membrane or mixed with the contents of the 
organ. It has, in rare cases, been found encysted in the stomach in 
considerable quantity. "When invisible to the naked eye a micro- 
scopical examination of the stomach contents will not infrequently 
reveal characteristic crystals of arsenious acid or some of its com- 
pounds. The stomach may be contracted and its mucous membrane 
corrugated. The entire inner surface may be red and inflamed, or 
there may be patches or streaks of inflammation or deep congestion. 
The inflamed and congested patches may be thickened and covered 
with false membrane mixed with larger and smaller particles or 
masses of the poison. Ulceration, perforation, and gangrene are 
rare. Blood may be extravasated into the mucosa and submucosa, 
and with the congestion give the mucous membrane a very dark-red 
or brown appearance. Frequently the mucous membrane is studded 
with small petechise. Sometimes the arsenic is converted in the 
stomach into the yellow sulphide. There may be acute gastritis, 
even when the poison is absorbed by the skin or otherwise and not 
introduced into the stomach. Taylor mentions a case in which the 
coats of the stomach were thickened and gelatinous, but not con- 
gested. The epithelium of the gastric glands may undergo granular 
and fatty degeneration. 

The entire length of the intestine may be congested and inflamed, 
but the action of the poison does not usually extend beyond the duo- 
denum. In some cases the solitary lymph nodules, Peyer's 
patches, and the mesenteric nodes are swollen. Inflammation of 
the bladder and peritoneum, and congestion and oedema of the 
brain, have been observed, but are neither frequent nor in any way 
characteristic. 

Fatty degeneration of the muscles, liver, kidneys, blood vessels, 
and vesicular epithelium of the lungs may be produced in arsenical 
poisoning. 

Alterations in the spinal cord indicative of acute myelitis have 
been described by Popon l as occurring in dogs poisoned with arse- 
nious acid. 

The walls of the stomach and intestines and other parts of the 
body may be preserved from decomposition for a long time after 
death by arsenical poisoning. 

It should always be borne in mind, in examining cases of sus- 

1 Popon, ' ' Ueber die Veranderungen im Rlickerimarke nach Vergif tung mit Arsen, " 
etc., Virch. Arch., Bd. xciii., p. 351. 



820 DEATH FROM POISONING. 

pected arsenical poisoning, that death may be produced by arsenic 
and its compounds without any appreciable lesions. While in gene- 
ral it may be said that in the cases in which no lesions are discovered 
death has been rapid, the death may be delayed in such cases until 
long after a period at which, in other cases, marked inflammatory 
changes have occurred. 

Compounds of arsenic, such as the chloride and sulphide, and the 
arsenite (Scheele's green, Paris green), are sometimes used for sui- 
cidal purposes, and produce lesions similar to those of arsenious 
acid. Paris green is a favorite article in New York, particularly 
among Germans, for suicidal purposes. It is usually taken in con- 
siderable quantities, and is often found in the stomach after death. 1 

CORROSIVE SUBLIMATE. 

The mucous membrane of the mouth and throat may be swollen, 
inflamed, or have a grayish-white appearance. The oesophagus may 
be swollen and white, or congested, or unaltered. The mucous mem- 
brane of the stomach is usually congested or inflamed, or there may 
be patches of softening, ulceration, or gangrene. Perforation is of 
rare occurrence. Small ecchymoses in the mucosa are not uncom- 
mon. Sometimes there is little or no change in the stomach. Some- 
times the mucous membrane of the stomach is slate-colored from the 
deposition of metallic mercury from the decomposed salt. The in- 
testines may appear normal, or there may be patches of congestion 
and ecchymosis. 

The larynx and trachea may be congested. The kidneys may 
show parenchymatous and fatty degeneration of the epithelium. 



LEAD. 

The different preparations of lead may prove fatal either from 
the immediate effect of large doses or from the gradual effects of re- 

1 It is advisable, in cases of suspected arsenic poisoning, particularly if the body 
have lain for some time, as in exhumations, to preserve not only all of the internal 
organs entire for the chemist, but also portions of the muscles (back, thigh, arm, and 
abdomen), and also one of the long bones, preferably the femur, since arsenious acid 
and its compounds are quite diffusible, and may be present in proportionately larger 
quantity in other parts than in the gastro-intestinal canal. It is desirable to save the 
whole of the internal organs, and to weigh the muscle and bones as well as the whole 
body at the autopsy, in order that the calculations of the chemist, in case arsenic be 
found, may rest upon a definite basis, and be as little as possible dependent upon esti- 
mates, whose value may be questioned by lawyers should the case come into the 
courts. 

An interesting article on arsenic as a poison, with various collateral data by 
Pellew, will be found in Hamilton's " System of Legal Medicine, " vol. i., p 349. 



DEATH FROM POISONING. 821 

peated small doses. Although there may be marked symptoms dur- 
ing life, the post-mortem lesions are few and variable. 

Large doses may produce acute gastritis, and sometimes a whiten- 
ing of the mucous membrane. The intestines are generally con- 
tracted, and there may be fatty degeneration of the renal epithelium ; 
very frequently there are no appreciable lesions. 

In chronic lead poisoning the intestines may be contracted, the 
voluntary muscles flabby and light-colored, or partially replaced by 
connective tissue, and there may be chronic meningitis. 

COPPER. 

Acute poisoning by salts of copper is not very common, but it is 
of occasional accidental occurrence, and the salts are infrequently 
used with suicidal intent. The sulphate and acetate are the most 
important salts in this respect. Soluble salts of copper may be 
formed in the use of copper cooking utensils, and accidents most fre- 
quently occur in this way. 

The post-mortem appearances are somewhat variable. The 
pharynx and oesophagus may be somewhat inflamed or unchanged. 
The mucous membrane of the stomach and intestines may be in- 
flamed, ulcerated, or gangrenous, and perforation and peritonitis 
may occur. The mucous membrane may have a diffuse greenish 
color, or particles of the salt may be found adhering to it. 

TARTAR EMETIC. 

This preparation of antimony may prove fatal when administered 
in a single large dose or in repeated small doses. The post-mortem 
lesions are not constant. In cases of chronic poisoning there are 
usually no appreciable lesions. 

In cases of acute poisoning there may be evidence of acute in- 
flammation of the oesophagus, stomach, intestines, and perito- 
neum. Sometimes the stomach exhibits no lesions, while the intes- 
tine is involved. The larynx and lungs may be deeply congested. 



VEGETABLE IRRITANTS. 

Aloes, colocynth, gamboge, jalap, scammony, savin, croton 
oil, colchicum, veratria, hellebore, elaterium, and turpentine. 

All these drugs may produce poisonous effects. The post-mortem 
lesions are congestion, inflammation, and sometimes ulceration of 
the gastro-intestinal mucous membrane ; but these lesions are some- 
times present and sometimes absent. 
64 



822 DEATH FROM POISONING. 



CANTHAEIDES. 



This substance may be given in powder or tincture. The entire 
length or only a portion of the alimentary canal may be congested 
or inflamed. There may be patches of gangrene of the mucous 
membrane of the stomach. When the poison was taken in sub- 
stance a microscopical examination of the contents of the alimentary 
canal or of the mucous membrane may reveal the glistening green 
and gold particles of the fly. 

The kidneys, ureters, and bladder may be congested and in- 
flamed. There is sometimes congestion of the brain and its mem- 
branes. 

OPIUM. 

The post-mortem appearances in persons who have died from 
opium poisoning are inconstant and not characteristic. Congestion 
of the brain and its membranes, with serous effusion in the mem- 
branes and ventricles, and congestion of the lungs, are changes oc- 
casionally seen, but they are frequently entirely absent, and when 
present are not characteristic of death from this poison. 

POISONOUS FUNGI. 

The action of these substances varies greatly, and the post-mor- 
tem appearances are inconstant and not characteristic. In general, 
when any lesions are present, they are those of gastro-intestinal irri- 
tation or of venous congestion, or both. 

Microscopical examination may reveal characteristic fragments of 
fungi in the contents of the alimentary canal. 

HYDROCYANIC ACID. 

This poison in fatal doses may destroy life in a very short time. 
The post-mortem appearances are inconstant and not characteristic. 
The skin may be livid and the muscles contracted. The stomach 
may be congested or normal. The most frequent internal appear- 
ances are those of general venous congestion. Under favorable con- 
ditions the odor of prussic acid may be detected in the stomach or 
blood or brain, or other parts of the body. It may be absent in the 
stomach and present in other parts of the body. If the patient have 
lived for some time the odor ma}' be absent altogether. 

Cyanide of potassium may produce the same lesions as prussic 
acid, and there is the same inconstancy in their occurrence. 

Nitrobenzole. — This substance produces general venous conges- 



DEATH FROM POISONING. 823 

tion, and the odor of the oil of bitter almonds may be more or less well 
marked in the body after death. 



CAEBOLIC ACID. 

When this poison is taken into the stomach the mucous mem- 
brane of the mouth, oesophagus, and stomach may be white, cor- 
rugated, and partially detached in patches, and the edges of the 
affected parts may be hypersemic or there may be patches of extra- 
vasation. Brownish, shrunken patches may be present about the 
mouth. The brain and meninges may be congested. There may 
be congestion and cedema of the lungs, and congestion of the liver 
and spleen. The blood is usually dark and fluid. The urine is 
usually of a dark or greenish color. The odor of the poison may be 
evident in the body and in the urine. 

ALCOHOL. 

The different preparations of alcohol, when taken in concentrated 
form or in large quantities, sometimes produce sudden coma and 
death in from half an hour to several hours. In acute poisoning, if 
death have followed soon after the ingestion of the poison, the body 
may resist decomposition for an unusual length of time. The stomach 
and tissues may even have a more or less well-marked alcoholic odor. 
The stomach, and even the oesophagus and duodenum, may be of a 
deep-red color. There may be punctiform ecchymoses in the gastric 
mucous membrane. In many cases the stomach is apparently quite 
normal. There is apt to be venous congestion in some of the internal 
organs, but this is not constant. There is frequently congestion and 
sometimes extravasation of blood in the brain and its membranes, 
and cedema of the membranes or of the brain substance, or both. 
There may be a serous effusion in the ventricles of the brain. The 
bladder is frequently distended with urine, as in other cases in which 
death is preceded by a period of unconsciousness. 

Chronic alcohol poisoning is of a different nature. The subjects 
of it may die from some other disease, or they die after a debauch 
without anything else to account for their death. In the latter case 
there may be delirium tremens, or the patient dies exhausted and 
comatose. Chronic alcoholism is not infrequently mistaken clinically 
for meningitis. The post-mortem lesions are sometimes marked, 
sometimes absent. There may be chronic pachymeningitis, resulting 
in thickening of the dura mater and its close adherence to the skull. 
The pia mat.er may be thickened and cedematous. The brain may 
be normal or cedematous or atrophied. The lungs are frequently 



824 DEATH FROM POISONING. 

congested. The heart may be thickly covered with fat, and its walls 
may be flabby and fatty. The stomach frequently presents the 
lesions of chronic gastritis. The liver may be cirrhotic, with or with- 
out fatty infiltration. The kidneys may present the lesions of paren- 
chymatous or fatty degeneration or of chronic diffuse nephritis. 

It should always be remembered, however, that all or a part of 
the above lesions may be absent in the bodies of drunkards, and,, 
furthermore, that the same lesions may be due to other causes. 

CHLOROFORM. 

Chloroform may cause death when it is taken in fluid form into 
the stomach or when inhaled. Death from swallowing liquid chlo- 
roform is rare, and its immediate cause is usually uncertain. The 
post-mortem changes are variable ; sometimes there are no lesions. 
In some cases there is simple reddening of the gastric mucous mem- 
brane ; occasionally there is acute gastritis or ulceration of the mu- 
cous membrane. The odor of chloroform may or may not be evi- 
dent. Discoloration and softening of the mucous membrane of the 
pharynx, oesophagus, and duodenum have been observed. There 
may be general venous congestion ; the heart may be flabby. Bub- 
bles of gas have been frequently seen in the blood, but this is not 
characteristic. Death from inhalation of chloroform is a not infre- 
quent accident in surgical practice. After death from inhalation 
the results of the examination are usually quite negative. 

ETHER. 

The inhalation of ether occasionally causes death. The post- 
mortem examination is negative. The ingestion of fluid ether may 
induce inflammation of the stomach. The odor of ether may be per- 
ceptible if the autopsy is made soon after death. 

CHLORAL HYDRATE. 

There are no characteristic post-mortem appearances after death 
by chloral. Hypersemia of the brain, and the odor of the drug, have 
been noticed. 

STRYCHNIA— NUX VOMICA. 

The post-mortem appearances after poisoning by these drugs are- 
not characteristic and are inconstant. The body is usually relaxed 
at the time of death, but the rigor mortis usually comes on early and 
remains long. There may be congestion of the brain and spinal 
cord, and sometimes of the lungs and stomach. 



DEATH FROM POISONING. 825 



CONIUM, ACONITE, LOBELIA INFLATA, DIGITALIS, STRAMONIUM. 

These vegetable poisons are administered in their natural form of 
leaves, berries, and roots, or in tinctures, infusions, and extracts, or 
in the form of their active alkaloid principles. 

If the leaves, berries, or seeds are given they may be detected in 
the contents of the stomach by microscopical examination. Other- 
wise the results of autopsies are hot characteristic. 

The brain and its membranes, and the lungs, may be congested. 
The stomach may present patches of congestion, inflammation, and 
extravasation, or its entire mucous coat may be inflamed, or it may 
appear normal. 

Microscopical examination of the contents of the alimentary canal 
may reveal characteristic seeds or fragments of leaves. 1 



PTOMAINES AND OTHER PUTREFACTIVE PRODUCTS. 

The effects upon the tissues of various forms of bacterial poisons 
liave been considered in the section on Infectious Diseases and else- 
where. Too little is as yet known of the chemistry of these toxic 
products to render their systematic consideration at all satisfactory. 
But it seems likely that these products may have medico-legal bear- 
ings which will in the future make their consideration of importance 
in certain cases of death from obscure causes. 2 



CARBONIC OXIDE. 

This is one of the gases formed in the burning of charcoal, and 
forms one of the ingredients of illuminating gas. The most charac- 
teristic post-mortem appearance is the cherry-red color of the blood, 
and of the tissues and. viscera which contain blood. The presence of 
carbonic acid in the gas may obscure the bright red of the carbonic 
oxide by the dark color which it induces in the blood. 

CARBONIC ACID. 
The lesions are essentially those of asphyxia, but the brain is said 

1 Consult Guy and Ferrier, "Principles of Forensic Medicine, " 7th ed., 1895. 

2 For certain chemical aspects of this newly opened field in toxicology consult 
Vaughan in Hamilton's "System of Legal Medicine, " vol. i., p. 475, and Vaughan 
and Novy, "Ptomaines and Leucomai'nes, ".3d ed., 1896. 



826 



DEATH FROM POISONING. 



to be more frequently congested than in asphyxia by simple obstruc- 
tion of respiration. 

For a more detailed consideration of poisons, their effects, modes of detection, 
etc., consult Taylor on Poisons; Maschka's "Handbuch der gerichtlichen Medicin, " 
Bd. ii. ; Woodman and Tidy, "Forensic Medicine." Wormley's "Micro-chemistry 
of Poisons" contains a series of good plates of the microscopical appearance of vari- 
ous forms of crystals of poisonous substances. 

Lesser' s " Atlas der gerichtlichen Medicin" contains a series of fine colored plates 
showing the appearance of the stomach after the action of various poisons. The 
work of Guy and Ferrier on "Forensic Medicine, " 7th ed. revised by Smith, con- 
tains in very compact and reliable form much information on the general subjects 
treated in the foregoing section. 



INDEX. 



Abbot, bacteriology, ref., 182 

and Ghiriskey, diphtheria in animals, 

ref., 253 
rhinitis, membranous, ref., 538 

Abel, capsulated bacillus, ref., 260 
ozeena, ref., 538 

Abdomen, examination of portion of, 22, 30 

Achard and Phulpin, bacteria in body after 
death, 167 

Achorion Schonleinii, 169 

Acid, carbolic, poisoning, lesions of, 823 
carbonic, poisoning, lesions of, 825 
hydrochloric, poisoning, lesions of, 816 
hydrocyanic, poisoning, lesions of, 822 
nitric, poisoning, lesions of, 815 
osmic, use of, in preserving tissues, 54 
oxalic, poisoning, lesions of, 816 
picric, use of, in decalcifying, 52 
sulphuric, poisoning, lesions of, 814 
tartaric, poisoning, lesions of, 816 

Aconite poisoning, lesions of, 825 

Acrania, 387 

Acromegalia, 410 

Abscess, 124 

of the brain, 381 

Actinomyces, 262 

Actinomycosis, 262 

Addison's disease, 800 

Adenie, 796 

Adenoid polyp of pharynx, 544 

Adenoma, 328, 330 

Adrenals, examination and preservation, 
32 
lesions of, 644, 801 

Aerobic bacteria, 148 

Agar, nutrient, 160 

Aguillula, 141 

AMfeldt. placental cysts, ref., 734 

Akerlund, membranous enteritis, ref., 564 

Albumen fixative, 59 

Alcohol, as preservative and hardening 
agent, 19, 52 
poisoning, 823 

Alexander, lymph nodules in bladder, 
ref., 684 



Alexander, adrenals and nervous system, 

ref., 644 
Alexins, 178 
Alimentary canal, 533 
Aloes poisoning, 821 
Ammonia poisoning, 817 
Amoeba coli, 127, 569 

colitis, 569 

dysenterica, 127 
Amyelia, 405 
Amjdoid degeneration, 100 

degeneration, tests for, 32, 35, 101 
Amyotrophic lateral sclerosis, 396 
Anaemia, 69, 77 

changes of blood in, 79 

infantum pseudo-leukaemica, 797 

of children, 797 

pernicious, 792 

pernicious, changes of blood in, 79, 793 
Anaerobic bacteria, 148 
Anencephalia, 387 
Aneurism, aortic, 512 

cirsoid, 509 

dissecting, 515, 516 

false, 515 

heart, 500 

miliary, of brain, 375 

minute, of brain, 15 

multiple, 507 
Angina, membranous, 204 
Angiocholitis, 617 
Angioma, 324, 326 
Anhydrseniia, 76 

Anilin-gentian-violet solution, 156 
Animals, infectious diseases of, 285 
Anthrax, 209 

bacillus of, 210 

immunity, artificial, in cattle, 212 

intestinalis, 577 
Antitoxin, 181 

diphtheria, 253 

pneumonia, 202 

streptococcus, 193 

tetanus, 256 
Aorta, aneurism of, 512 



828 



INDEX. 



Aorta, inflammation of, 508 
Aphthae, 170 
Apoplexy, brain, 374 

serous, 373 
Appendicitis, 573 

bacteria in, 575 
Appendix vermiformis, tumors of, 575 
Archiblast and parablast, relation of tu- 
mors to, 294 
Amdt, peritonitis, ref., 583 
Arnold, acromegalic, ref., 410 

hairy polyps of pharynx, ref., 543 

lymphatic tissues in liver, ref., 614 
Arsenic poisoning, lesions of, 818 
Arteries, atheroma of, 509 

dilatation of, 509 

inflammation of, 503, 509 

rupture of, 514 

sclerosis of, 507 

stenosis of, 513 

terminal character of. 74 

tumors of, 516 

wounds of, 514 
Arteritis, 503 

aneurisms of, 509 

chronic, 504 

obliterating, 505 

tuberculous, 509 
Arthritis, acute, 775 

chronic, 776 

deformans, 776 

gouty, 777 

tuberculous, 777 
Arthropods, 141 

Arthrogenous spores in heart, 147 
Ascaris, 136, 141 

Aschoff, parenchyma-cell emboli, ref., 73 
Asiatic cholera, 265 

Askanazy, endothelioma of kidney, ref., 680 
Asphyxia, 809, 813 
Atelectasis of lungs, 436 
Atelomyelia, 405 
Atheroma of arteries, 509 
Autopsies, medico-legal, 41 

method of making, 3 

Babes, hydrophobia, ref., 276 
Bacillus, 144 

aerogenes capsulatus, 193, 261 

anthracis, 210 

coli communis, 193, 260 

diphtherias, 250 

lepras, 230 

mallei, 235 

cedematis maligni, 259 

of bubonic plague, 239 



Bacillus of influenza, 257 

of measles, 274 

pneumoniae (Friedliinder), 259 

proteus, 193, 261 

pyocyaneus, 193, 261 

pyogenes, 193 

pyogenes fcetidus, 193 

pyogenes soli, 193 

rhinoscleromatis, 238 

tetani, 255 

tuberculosis, 213, 215 

typhi abdominalis, 240, 246 
Bacteria, 143 

action of cold on, 148 

action of heat on, 148 

action of, in the body, 172, 173, 174 

aerobic, 148 

anaerobic, 148 

blood serum as culture medium for, 
162 

capsules of, 146 

changes in the body induced by, 172 

chromogenic, 150 

classification of, 153 

collection of, by sterilized swab, 166, 
167 

colonies of, 159 

cultivation of, 158 

culture medium for, 159 

disinfectants, action on, 149 

distribution in nature, 151 

Esmarch's soil culture of, 166 

examination for, at post mortems, 167 

fermentations by, 150 

forms of, 144 

growth, forms of, 145 

importance, relative, of, in disease, 175 

in fluids, to stain, 154 

in tissues, to stain, 156 

in water, 151 

light, action of, on, 11, 19 

method of staining, Gram's, 156 

method of study of, 154 

morphological examination of, 154 

nitrifying, 150 

nutrition and functions of, 148 

parasites, 152 

Petri plate culture of, 163 

photogenic, 150 

plate culture of, 163 

proof of relation of, to disease, 175 

protective mechanism of the body 
against, 171 

putrefaction by, 150 

relations of, to diseases, 171 

role of, in nature, 149 



INDEX. 



829 



Bacteria, safeguards of the body against, 
171 

saprophytic, 152 

solid media for cultivation of, 159 

spore staining in, 155 

spores of, 147 

staining of, 151 

thermophyllic, 148 
' various forms of, 152 

varieties in, 147 

zymogenic, 150 
Bacterial emboli, 172 

inoculations of animals, 166 
Bacterio-protein, 173 

Bailey and Ewing, Landry's paralysis, 400 
Bailey's knife for division of spinal cord, 

12 
Balanitis, 743 
Balantidium coli, 129 
Barker, malaria, ref., 283 

Flexncr and, meningitis, ref., 200 
Baumgarten, " Jahresbericht," ref., 182, 226 
Basedow's disease, 643 
Beck, influenza bacillus, ref., 258 
Beebe, Park and, diphtheria, ref., 252 
Benecke, 73 

Bergeron, stomatite ulcerosa, ref., 534 
Berkley, nerve lesions, ref., 377 
Berry, appendicitis, ref., 575 
Berthenson, heart tumors, ref., 502 
Biedl and Kraus, bacteria eliminated from 

the body, 178 
Biggs, Park, and Beebe, diphtheria, bacteri- 
ological diagnosis in, ref., 254 
Biliary calculi, 619 

passages, inflammations of, 617 
Birch-Hirschfeld, epithelioma of pleura, 

ref., 426 
Bladder, urinary, bacteria in, 685 

calculi, 687 

dilatation of, 681 

displacements of, 681 

diverticula of, 682 

haemorrhage of, 683 

herniae of, 682 

hyperemia of, 683 

inflammation of, 683, 685 

lesions of, 680 

malformations, 680 

parasites of, 687 

perforation of, 682 

rupture of, 687 
Blood, air in, 90 

alkaline changes in, 76 

anaemia, pernicious, 792 

chlorosis, 791 



Blood composition, alterations of, 791 

changes in, after extravasation, 71 

changes in circulation of, 69 

changes in structure of, 77 

circulation of, changes of, in inflamma- 
tion, 111 

clots in heart, 27 

coagulability, changes in, 76 

coagulation of, in body after death, 10 

composition of, changes in, 76 

distribution of, in body after death, 10 

examination, morphological, 86, 87 

extravasation of, 69, 70 

fat in, method of staining, 89 

foreign bodies in, 89 

leukaemia, 794 

plethora, 77 
Blood cells, diapedesis of, in inflamma- 
tion, 112 

red, changes in, 77 

red, nucleated, 81 

red, regeneration of, 95 

white, changes in, 82 

white, forms of, 82 

white, regeneration of, 95 
Blood serum, as culture medium, 162 

immunization, 181 
Blood, staining methods, 88 
Blood vessels, atrophy of, 502 

brain, preservation of, 19 

calcification of, 503 

degeneration of, 503 

formation of new, 121 

hypertrophy, 502 

inflammation of, 503 

volume of, increase of, 77 
Bone, abscess, 761 

atrophy, 771 

caries, 766 

dislocations, 754 

fractures, 754 

haemorrhage, 754 

healing of fractures of, 125 

hyperaemia, 754 

inflammation, 755 

necrosis, 765 

parasites, 774 

tumors, 771 

wounds, 754 
Bone marrow, alterations of, in anaemia,770 

alterations of in leukaemia, 770 
Bolton, Bacillus pyogenes soli, ref., 193 
Bordoni-Uffreduzzi, cultivation of lepra 

bacillus, 230 
Bothriocephalus, 135 
Brain, abscess, 381 



830 



INDEX. 



Brain, anaemia of, 373 

atrophy of, 378 

axis, method of separation of, 17 

changes in toxaemia, 376 

cysts in, 380, 387 

degeneration of, 371 

dura mater, 347 

embolism, 370 

haemorrhage in, 379 

hernia of, 388 

holes in, 380 

hyperemia of, 373 

hypertrophy of, 378 

inflammation of, 380, 382 

inflammation in new-born, 383 

inflammation, syphilitic, 384 

inflammation, tuberculous, 384 

malformations of, 387 

Meynert's method of dissection, 15 

oedema of, 373 

parasites in, 387 

paresis, lesions of, in, 385 

pia mater, 352 

pigmentation, 86 

post-mortem examination and preser- 
vation of, 11, 13, 15, 17, 18 

sand, 368 

sclerosis of, 382 

secondary degeneration of, 377 

softening, 381 

thrombosis, 370 

tumors of, 386 

ventricles, 365 

weight of, 12 

wounds of, 379 
Bramann, cysts of mesentery, ref., 589 
Brannan and Cheesman, typhus fever, ref M 

275 
Brens, cysts of myomata, ref., 712 
Bright' s disease, acute, 650, 655 

chronic, 659, 660, 668 
Brigidi and Piccoli, persistent thymus, ref., 

643, 796 
Brockway, specimen of trichocephalis dis- 

par, 138 
Bronchi, examination and preservation of, 
28, 29 

inflammation of, 426 

tumors of, 431 
Bronchiectasia, 429 
Bronchiolitis exudativa, 429 
Bronchitis, croupous, 429 

acute catarrhal, 426 

chronic catarrhal, 428 
Broncho-pneumonia, 443 
Broth, nutrient, 161 



Brown induration, 449 

Bruises, post-mortem, appearance of, 8 

Buboes, 524 

Bubonic plague, 239 

Bulbar paralysis, 396 

Burning, death from, 807 

Butler, membranous enteritis, ref., 564 

Byron, cultivation of lepra bacillus, 230 

Cadaveric lividity, 5 

Caecum, 573 

Calcareous degeneration, 105 

Calcification, 105 

Calculi, biliary, 619 

renal, 677 

urinary, 687 
Calvarium, method of opening of, 10 
Campbell, pharyngo-mycosis, ref., 284 
Cancer of brain, 351 
Canon, bacteria in sepsis, ref., 197 

Pfeifer, Kitasato and, influenza bacillus, 
ref., 257 

and Pielicke, bacillus of measles, ref., 
274 
Cantharides poisoning, 822 
Capillaries, blood, 520 
Capillary bronchitis, 443 
Capsules, suprarenal, 32 
Carbonic oxide poisoning , 825 
Carbuncle, 209 
Carcinoma, 331 

alveolar, 342 

cells, 334 

colloid, 341 

epithelial pearls in, 340 

forms of, 336 

genesis of, 328, 333 

metastasis in, 334 

myomatous, 343 

relation of sporozoa to, 129 
Caries, 766 
Carnoy's fluid, 50 
Caspar, description of foetus, 42 
Catarrhal fever, 257 

inflammation, 114 
Cell division, 92 

nucleus, changes in, during division, 92 
Cells, epithelioid, in granulation tissue, 122 

new, in inflammation, 109 

pus, 117 
Celloidin as embedding agent, 56 
Cephalocele, 388 
Cercomonas intestinalis, 129 
Cerebro-spinal meningitis, bacteria in, 200 
Cestoda, 131 
Chancre, 233 



INDEX, 



831 



Charbon, 209 

Charcot's crystals, 85 

Chemotaxis, 149, 175 

Cheesman and Brannan, typhus fever, rei. 

275 
Cheesy degeneration, 97 
Chest serum as cultivating medium for 

bacteria, 162 
Chiari, infarction of uterus, ref., 703 
Chloral hydrate poisoning, 824 
Chloroform poisoning, 824 
Chloroma, 312 
Chloiosis, 791 
Cholecystitis, 617 
Cholera, Asiatic, 265 
Cholesteatoma, 315 
Chondroma, 317 

Choroid plexus, lesions of, 14, 365 
Chromic and acetic acid mixture of Flem- 

ming, 64 
Chromosomes, 93 

Cicatrices, post-mortem appearance of, 9 
Cicatrix, formation of, 123 
Circulation, changes in, 69 
Cirrhosis, hypertrophic, of liver, 605 

of kidney, 668 

of liver, 604 
Clostridium forms of bacteria, 144 
Clots of heart, pre-examination of, 27 
Cloudy swelling, 98 
Coagulation necrosis, 96 

of blood in heart, 27 
Cobbold, entozoa of man, 142 
Cocci, 144 

Coccidium oviforme, 128 
Colchicum poisoning, 821 
Colitis, amoebic, 569 

bacteria in. 572 

catarrhal, acute, 563 

chronic, 573 

croupous, 567 

follicular, 568 

membranous, 564 

necrotic, 572 
Colloid degeneration, 103 

carcinoma, 341 
Colocynth poisoning, 821 
Colon bacillus, 260 
Comma bacillus, 266 
Commensals, bacterial, 152 
Concurrent infection in tuberculosis, 224 
Condyloma, syphilitic, 233 
Congestion in inflammation, 108 
Cohnheim, theory of origin of tumors, 290, 
332 

on infarction, 74 



Conium poisoning, 825 

Contagious diseases, 187 

Contusions, post-mortem appearance of, 7 

Cooling, post-mortem rate of, 6 

Copper, poisoning by, 821 

Cornil, myelocytes, 85 

Corpora aliena articulorum, 779 

amylacea, 101 
Corrosive sublimate fixative agent, 55 

sublimate poisoning, 821 
Councilman, sudden death from heart, ref., 
487 

and Lafleur, on amoebic dysentery, 182 
Courty, hymen, lesions of, 692 
Cowper's glands, 753 
Cramer, sunstroke, ref., 806 
Craniotabes, 768 
Croton oil poisoning, 821 
Cryptogenetic pyaemia, 197 
Cryptorchismus, 745 
Cultivation of bacteria, 158 
Cullen, rapid method of hardening, 51 
Cyclopia, 387 
Cylindroma, 316 
Cystitis, 683 
Cysts, 295 

ciliated, 297 

method of preserving, 64 

Darling, Bacillus coli communis, ref., 260 

David, bacteria of mouth, ref., 538 

Death, causes of, 3. 

Decalcification of bone, 51 

Decidua, remains of, in uterus, 718 

Deciduoma malignum, 717 

Deck plugs, for mounting specimens in 

celloidin, 57 
Decomposition, post-mortem, 495 
Defensive proteids, 178 
Degeneration, acute, 98 

amyloid, 100 

calcareous, 105 

cheesy, 97, 219 

coagulation necrosis, 96 

colloid, 103 

fatty, 98 

forms of, 96 

glycogen, 102 

granular, 98 

gray, of nervous system, 396 

hyalin, 104 

inflammatory, 107 

mucous, 102 

parenchymatous, 98 

secondary, of spinal cord, 393 
Degeneration, waxy, 100 



$32 



INDEX. 



Delafield's haematoxylin, 60 
Demonstration specimens, and preserva- 
tion of, 63 
Dentrites, 393 
Diabetes mellitus, 804 
Diapedesis, 70, 112 
Diastematomyelia, 405 
Digitalis poisoning, 825 
Dinwiddle, veterinary microbiology, ref., 

285 
Diphtheria, 250 

antitoxin of, 181, 250, 253 

heart lesions in, ref., 250 

pseud o, 204 

toxin, 253 
Diphtheroid-angina, 204 
Diplobacillus, 146 

pneumoniae, 193 
Diplococcus, 145 

intracellularis meningitidis, 200 

lanceolatus, 200, 201, 438 

pneumoniae, 438 
Diplomyelia, 405 
Discoloration, post-mortem, 5 
Distoma, 130 

Dittel, urethral strictures, ref., 689 
Dmochowskl and Janowski, adenoma of liver, 
ref., 612 

pyogenic powers of typhoid bacillus, 
ref., 247 
Dobrowolski, lymph nodules, ref., 540 
Dochmius duodenalis, 137 
Dock, chloroma, ref., 312 

trichomonas, 130 
Dowd, pyogenic bacteria in New York, 

ref., 192 
Dropsy, 71 
Drowning, 811 
Dunbar, Asiatic cholera, ref., 268 

typhoid fever, ref, 249 
Dunin, fragmentation of heart muscle, 

ref., 493 
Duodenum, removal, examination, and 
preservation of, 35 

ulcers of, 562 
Dura mater, 347 

examination and preservation of, 11, 18 

haemorrhage, 347 

inflammation, 348 

thrombosis, 348 

tumors, 351 
Dust, anthrax bacilli in, 309 

bacilli in, inducing tuberculosis, 223 

pyogenic bacteria in, 190 

Ear, internal, pre-examination of, 18 



Echinococcus, 132, 134 

multilocularis of liver, 615 

of liver, 614 
Ecchondroses, 318 
Ecchymoses, 8, 70 
Edebohls, hepatic abscess, ref., 602 
Edel, diverticula, false, intestines, ref., 577 
Eden, placental structure, ref., 733 
Edmunds, Basedow's disease, ref., 643 
Ehrlich, change in red blood cells, ref., 81 

and Birch-Hlrsehfeld, anaemia, ref., 77 
Ehrlich's method of fixing blood, 88 
Elaterium poisoning, 824 
Electricity, death from, 808 
Ely, diverticula of bladder, ref., 681 
Embedding in celloidin, 56 

in paraffin, 58 
Emboli, 73 

fat, 89 

parenchyma cell, 73 
Embolism, 73 

Embryo, human, size of, at various pe- 
riods, 42 
Emigration in inflammation, 109, 111 
Empyema, 421 
Encephalitis, 380 

chronic, 382 

in new-born, 383 
Encephalocele, 388 
Encephaloid cancer, 341 
Endogenous spores in bacteria, 147 
Endocarditis, acute, 494 

chronic, 496 

malignant, 494 

mycotic, 494 

tuberculous, 498 

ulcerative, 494, 498 
Endocardium, fatty degeneration of, 491 

post-mortem appearance of, 27 

staining process of, 27 
Endometritis, acute, 704 

chronic, 705 

croupous, 706 

syphilitic, 707 

tuberculous, 706 
Endothelioma, 312 
Enteroliths, 577 
Enzymes, bacterial, 150 
Eosin, use of, in tissue staining, 61 
Eosinophile cells, 82 
Ependyma, 365 

inflammation of, 365 

preservation of, 18 

tumors of, 368 
Ependymitis, 365 
Epispadias, 742 



INDEX. 



833 



Epithelioma, 336 

Epulis, 309 

Erysipelas, 194 

Esmarch roll culture, 166 

Ether poisoning, 821 

Eulenberg, Basedow's disease, ref., 643 

Eiving, Bailey and, Landry's paralysis, ref., 

400 
Exophthalmic goitre, 643 
Exostoses, 319 
Exudates, 72 

in inflammation, 110 
inflammatory disposal of, 115 
Eyes, post-mortem examination of, 18 

Fallopian tubes, displacement and disten- 
tion of, 730 

tubes, haemorrhage of, 731 

tubes, inflammation of, 731 

tubes, length of, 40 

tubes, malformation of, 730 

tubes, tumors of, 732 
Famine fever, 269 
Farcy, 235 

Farner, Basedow's disease, ref, 643 
Fatty degeneration, 98 

infiltration, 98 
Fenomenodes, placental cysts, ref., 734 
Ferguson, specimen of filaria, 140 
Fibrin, formation of, in inflammation, 114 
Fibroblasts, 122 
Fibroma, 299 
Fibrosis, 125 
Filaria, 140 

Finkler, pneumonia, ref., 257 
Fission fungi, 143 
Fistula, vesico-vaginal, 696 
Fistulee, recto-vaginal, 696 
Fitz, pancreas lesions, ref, 634 
Fixative, albumen, 59 

Flemming's chromic and acetic acid mix- 
ture, 64 

osmic acid mixture, 54 
Flexner, action of toxalbumins, ref, 173 

Bacillus pyogenes filiform is, ref, 193 
• bacteriological examination at autop- 
sies, ref, 168 

lympho-sarcoma, ref, 796 

neuro-epithelioma, ref., 340 

terminal infections, ref, 185 

typhoid bacilli, ref., 247 

and Barker, meningitis, ref, 200 

Welch and, Bacillus aerogenes capsu- 
lars, ref, 261 

Welch and, effects of diphtheria ba- 
cilli in animals, ref, 253 
53 



Foetal tissues, preservation of, 49 

Foetus, size of human, at various periods, 

42 
Foote, oysters and typhoid, ref, 249 
For mad, colon, large, ref, 558 
Formalin as preservative and hardening 

agent, 19, 54 
Fractures, healing of, 125 

post-mortem marks of, 9 
Fraenkel, endothelioma of pleura, ref, 426 

hydatid moles, ref, 735 

pneumococcus of, 201 
Freeborn, formula for picric acid fuchsin, 
62 

ovarian papillomata, ref, 728 
Freeman, milk and typhoid fever, ref.„ 

249 
Freudweiler, phlebitis, ref, 519 
Friedliinder's pneumococcus, 259 
Friedreich, muscle atrophy, ref., 786 
Frog, exudative innammation in, 110 
Frozen sections, 51 
Fuchsin, picro-acid, 61 
Fungi, poisonous, 822 

Gage's hseniatoxylin, 61 
Gall bladder, lesions of, 617 

tumors of, 620 
Gall ducts, innammation of, 617 

tumors of, 620 
Gamboge poisoning, 821 
Ganglion cells, changes of, in toxaemia, 376 
Gangrene, hospital, of vulva, 693 
Gastritis, catarrhal, acute, 547 

catarrhal, chronic, 547 

croupous, 549 

phlegmonous, 549 

suppurative, 549 

toxic, 550 
Gelatin, nutrient, 159 
Generative organs, female, 39, 692 

organs, male, 38, 741 
Gemto-urinary organs, post-mortem ex- 
amination of, 38 
Germs, 143 
Ghriskey, Abbott and, diphtheria in animals^ 

ref, 253 
Giant cells, 92, 218 
Gigantoblasts, 82 
Gill clefts, persistent, 538 
Glanders, 235 

Glands, agminated, of intestine, 561 
Glazier, trichina, ref, 142 
Glioma, 320 
Gliomyxoma, 321 
Glio-sarcoma, 321 



834 



INDEX. 



Glomerulonephritis, 650, 655, 660 
Glossitis, 537 
Gluge's corpuscles, 372 
Glycogen degeneration, 102 
Goitre, 639 

exophthalmic, 643 
Golden coccus, 189 
Goldscheider, puerperal fever, bacteria in, 

ref., 197 
Golgi, silver stain, 62 

hydrophobia, ref., 276 
Gonococcus, 206, 207 

bacterial associates of, 208 
Gonorrhoea, 206 
Gout, 802 

Graham, displacements of liver, ref, 591 
Gram's method of staining bacteria, 156 

method of staining bacteria, Weigert's 
modification of, 157 
Granulation tissue, 121, 124 
Granulomata, 397 
Graves' disease, 643 
Grawitz, lung infarctions, ref, 434 
Gregarine, 128 

Gross, tumors of male mamma, ref, 753 
Guarnieri, agar for pneumococcus, 201 
Guinea-worm, 140 
Gumma, 233 

Hemangioma, 326 
Hematocele, 746 

uterine, 703 
Hematogenesis, defective, 78 
Hematoidin, 78 
Hematolysis, excessive, 78 
Hematoma, 70 
Hematomyelia, 391 
Hematomyelopore, 391 
Hematophilia, 799 
Hematoxylin, Delafield's, 60 

Gage's, 61 

Heidenhain's iron of, 61 
Heraatozoon of malaria, 280 
Hemoglobinemia,' 77 
Hemorrhage by diapedesis, 70 

by rhexis, 69 
Hemorrhagic diathesis, 799 

infarction, 70 

infections, 799 
Hemosiderin, 78 

Halm, cysts of mesentery, ref, 589 
Halliburton, chemical physiology, ref, 174 
Hanging, 8, 810 
Hansemann, diverticula," false, of intestine, 

ref, 577 
Hardening of tissues, 52 



Hayem's method of fixing blood, 88 

solution in blood examination, 87 
Head, method of post-mortem examina- 

tion of, 10 
Healing, first and second intention, 125 

of wounds, 120 

regeneration of tissue in, 94 
Heart, abnormal size of, 485 

aneurism of, 500 

atrophy of, 487 

changes in position of, 485 

clots in, 27 

degeneration of, 490 

dilatation of, 489 

examination of, 25, 26, 28 

fat tissue of, atrophy of, 492 

fatty, 490, 492 

fragmentation of muscle of, 493 

hyperplasia of, fibrous, 500 

hypertrophy of, 487 

inflammation of, 494 

lipomatosis of, 492 

malformations of, 483 

malpositions of, 485 

parasites in, 502 

rupture of, 486 

softening of, 493 

thrombosis of, 501 

tumors of, 502 

valves, lesions of, 500 

valves, test for sufficiency of, 26 

vegetations, 494, 497 

weight of, 27 

wounds of, 486 
Heidenhain's iron hematoxylin, 61 
Heiman, chest serum, 162 

study of gonococcus, ref, 207 
Hellebore poisoning, 821 
Hepatic artery, lesions of, 593 

veins, 598 
Hepatitis, acute, 601 

chronic, 604 

syphilitic, 608 

tuberculous, 609 
Heppner, hermaphroditism, ref, 742 
Hermaphroditism, 742 
Hernia intestino-vaginalis, 696 

uterine, 702 

vesico-vaginalis, 695 
Hess, cysts, Ciliated, ref, 297 
Heterotopia, 406 

false, 407 
Hewetson, Thayer and, malaria, ref, 283 
Hintze and Lubarsch, elimination of bac- 
teria from body, 178 
Hodenpyl, actinomycosis of lung, ref, 263 



INDEX. 



835 



Hodenpyl, on appendicitis, ref., 575 

rapid method of hardening, 51 

tonsils, faucial, ref., 540 

Prudden and, action of dead tubercle 
bacilli, 222 
Hodgkin's disease, 796 
Hoffman, hermaphroditism, ref., 742 
Hofmeier, placenta, ref., 734 
Horseshoe kidney, 646 
Hospital fever, 275 
Houl, hemorrhagic infections, 799 
Hueppe on bacteriology, ref., 182 
Huetes, intestinal tumors, ref., 577 
Hun and Prudden, myxoedema, ref., 642 
Hyalin degeneration, 104 

thrombi, 72 
Hydatid moles, 304, 735 
Hydremia, 77 
Hydrencephalocele, 388 
Hydrocele, 745 
Hydrocephalus, 362, 367, 388 
Hydromeningocele, 388 
Hydromyelia, 405 
Hydronephrosis, 674 
Hydrophobia, 276 
Hydrothorax, 417 
Hydrorrhachis interna, 405, 406 
Hymen, 692 
Hyperemia, 69 
Hyperplasia, 91 

replacement, fibrous, 125 
Hypertrophy, 91 
Hyphomycetes, 143 
Hypoleucocytosis, 83, 84 
Hypophysis cerebri, 369 
Hypospadia, 741 
Hypostasis, post-mortem, 5 

Identification, post-mortem features to be 

noticed in, 4 
III, echinococcus of liver, ref., 615 
Immunity, 177 

artificial, 178, 179, 180 

forms of, 178 
Infarction, hemorrhagic, 70, 74 
Infarctions of lungs, 433 
Infection, 183 

and immunity, 177 

concurrent, 184 

congenital, 185 

mixed, 184 

terminal, 185 
Infectious disease, 183 

disease, communicability of, 185 

disease, conditions influencing occur- 
rence of, 176 



Infectious disease, definition of, 177 

disease, nature of, 183 

disease, non-communicable, 186 

disease, predisposition to, 176 

disease, hypoleucocytosis in, 83 

disease of animals, 285 

disease produced by the pyogenic bac- 
teria, 188 

inflammation, pseudo-membranous, 
204 
Infiltration, fatty, 98 
Inflammation, 107 

catarrhal, 114 

congestion in, 108 

croupous, 119 

degeneration in, 107 

diphtheritic, 120 

emigration in, 109, 111 

exudative, 110 

exudative fibrinous, 114 

exudative, hemorrhagic, 114 

exudative, mucous, 114 

exudative, purulent, 114 

exudative, serous, 114 

forms of, 110 

interstitial, 118 

necrotic, 107, 119 

productive, 117 

productive, reparative, 120 

pseudo-membranous, of mucous mem- 
branes, 204 

reparative, 120 

suppurative, 188 

syphilitic, 232 

transudation in, 109 

tuberculous, 215, 216, 220 
Influenza, 257 
Infusoria, 129 

Inoculation, protective, 181 
Insolation, 806 
Intestinal mycosis, 210 
Intestine, large, inflammation, 563 

small, emboli, 562 

small, inflammation, 561 

small, lesions of lymph nodules, 561 
Intestines, appearance of, at autopsies, 34 

atresia of, 558 

concretions in, 577 

diverticula of, 557, 577 

examination and preservation of, 36 

examination, post-mortem, of, 23, 30, 34 

incarcerations of, 558 

intussusception, 559 

malformations of, 557 

parasites in, 578 

post-mortem changes in, 34 



836 



INDEX. 



Intestines, preservation of, 35 

rupture of, 560 

transposition, 560 

tumors of, 575 

waxy degeneration of, test for, 35 

wounds of, 560 
Intoxication by bacterial products, 174 
Involution forms of bacteria, 144 
Iodin as test for amyloid in fresh tissue, 
32 

solution in Gram's stain, 157 

use of, in removal of sublimate from 
tissues, 55 
Itch insect, 141 

Jager, acute yellow atrophy of liver, ref., 
601 
meningitis, ref., 200 

Jail fever, 275 

Jakowski, pyocyaneus, ref., 261 

Jalap poisoning, 821 

Janeway, E. G., foreign body in portal 
vein, 594 

Janeway, T. C, reaction of culture media 
for pneumococcus, 202 

Janowski, inflammatory suppuration, bac- 
teria in, ref., 192 

Joints, inflammatory, 775 
loose bodies in, 779 
tumors of, 778 

Jordan, osteomyelitis, ref., 765 

Jores, formula for gross specimen preser- 
vation, 63 

Jiirgenson, air in the blood, ref., 90 

Justi, tumors of heart, ref., 502 

Karyokinesis, 93 

asymmetrical, ref., 93 
Karyomitosis, 93 
Kelynack, appendicitis, ref., 575 
Kidney, abscess, 671 

arterio-sclerotic, 668 

bacteria in, 671, 672 

Bright' s disease of, 647 

calculi of, 677 

cirrhosis of, 668 

congestion, acute, 647 

congestion, chronic, 658 

cysts of, 675 

degeneration, acute, 648 

degeneration, chronic, 659 

degeneration, granular, 668 

degeneration, parenchymatous, 648 

degeneration, waxy, tests for, 32 

displacements of, 646 

embolism of, 673 



Kidney, examination of, 31, 32 

fatty, 659 

hydronephrosis, 674 

inflammation of, 650 

malformations, 646 

parasites of, 680 

perinephritis, 676 

surgical, 672 

thrombosis, 673 

tumors of, 677 

waxy, 660 
Kinnicutt, Graves' disease, ref., 643 
Kitasato, Pfeiffer, Canon and, influenza ba- 
cillus, ref., 257 
Klebs, cysts of ovaries, ref., 727 

malformations of genital organs, ref., 
742 
Klemperer, pneumonia antitoxin, ref., 202 
Koch's culture media, solid, 159 

discovery of tubercle bacillus, ref., 226 

report on Asiatic cholera, ref., 268 
Koplik and Van Arsdale, osteomyelitis, ref., 

765 
Kossel, Bacillus pyocyaneus, ref., 261 
Kotlar, heart thrombus, ref., 502 
Kraus, Biedl and, bacteria, elimination of, 

from body, 178 
Kruse and Pasquale, intestinal microbes, 
ref., 573 

liver, micro-organisms in abscess of, 
ref., 603 
Kiichenmeister and Zilrn, parasites, 142 

La grippe, 257 

Landry's paralysis, Bailey and Ewing, ref., 

400 
Lang, chloroma, ref., 312 
Lang's solution, 55 
Langerhans, fat necrosis, ref., 634 
Laryngitis, 413 

Larynx, examination and preservation of, 
29 

inflammation, 413 

malformations, 413 

tumors of, 416 
Lead poisoning, 820 
Legry, lung stones, ref., 423 
Leiomyoma, 321 
Lepra, 229 

bacillus, 230 
Leprosy, 229 
Leptothrix, 145, 146, 284 
Leptomeningitis, 354 
Leuckart, parasites, 142 
Leucocytes, changes in, 82 

degeneration of, in blood, 86 



INDEX. 



837 



Leucocytes, emigration of, in inflamma- 
tion, 112 

fate of, in inflammatory exudates, 
116 

formation, of, 95 

forms of, 82 
Leucocythaemia, 794 
Leucocytosis, form of, 83 

in infectious disease, 83 
Leukaemia, 794 

changes in blood cells in, 85 

pseudo-, 796 
Lewin and Heller, scleroderma, ref., 410 
Lipaemia, 89 
Lipoma, 317 

Lividities, post-mortem, 5 
Liver, abscess of, 601 

abscess, micro-organism in, 602 

amyloid, 597 

amyloid, tests for, 37 

anaemia, 591 

atrophy of, 595 

atrophy, acute yellow, 600 

bronze, 599 

cirrhosis of, 604 

congestion of, 591 

cysts of, 612-614 

degenerations of, 598 

discoloration, post-mortem of, 37 

examination and preservation of, 36 

examination, post-mortem, 23 

fatty, 596 

haemorrhage of, 593 

holes in, 614 

hyperemia, 591 

inflammation of, 601 

lymphatic tissue, hyperplasia of, 611 

malformations of, 590 

nutmeg, 605 

parasites of, 614 

pigmentation of, 599 

portal vein, lesions of, 593 

position of, 36 

position of, changes in, 24, 590 

preservation of, 37 

regenerative powers of, 95 

rupture of, 593 

size and weight of, 36 

tumors of, 612 

veins, lesions of, 595 

waxy, 597 

wounds of, 593 
Lobelia poisoning, 825 
Lockjaw, 255 
Locomotor ataxia, 402 
Loffler's alkalin-'methyl-blue stain, 158 



Loffler's blood serum mixture as culture 

medium, 162 
Loomis, gumma of heart, ref, 502 
Lbwit, oedema of lungs, ref, 433 
Lubarsch, Addison's disease, ref, 801 

endothelioma of kidney, 680 

and Hintze, elimination of bacteria 
from body, ref., 178 

and Ostertag's " Ergebnisse," etc., ref., 
182 
- Lungs, atelectasis of, 436 

congestion of, 432 

emphysema of, 434 

examination and preservation of, 28, 29 

gangrene of, 437 

haemorrhage of, 433 

hepatization of, 439 

hypostatic congestion of, 433 

infarctions of, 433 

inflammation of, 438 

inflammation, syphilitic, of, 475 

inflammation, tuberculous, of, 452 

injuries of, 432 

malformations of, 432 

oedema of, 432 

organized tissues in air vesicles of, 441 

parasites in, 477 

perforations of, 432 

phthisis, acute, 459 

phthisis, chronic, 469 

tuberculous, 452 

tuberculous, miliary acute, 453 

tuberculous, miliary chronic, 457 

tuberculous, miliary subacute, 456 

tumors of, 476 
Lung stones, 423 
Lupus, 227 

Lustgarten's bacillus, 234 
Lymphangiectasis, 522 
Lymphangioma, 327, 522 
Lymphangitis, 521 
Lymph glands, see Lymph nodes, 522 

nodes, 522 

nodes, degeneration in, 527, 536 

nodes, hyperplasia of, 531 

nodes, inflammation of, 523 

nodes, inflammation of syphilitic, 529 

nodes, parasites of, 532 

nodes, pigmentation of, 526 

nodes, scrofulous inflammation of, 528 

nodes, tuberculous inflammation of, 
528 

nodes, tumors of, 532 

nodules, intestinal, 561 

nodules of larynx, oesophagus, etc., 
ref, 540 



838 



INDEX. 



Lymph vessels, 520 

vessels, inflammation of, 521 

vessels, tumors of, 522 
Lymphocytes, forms of, 82 
Lymphocytosis, 85 
Lymphoma, 531 

Malarial fevers, 280 
Malignant pustule, 309 
Mamma, inflammation of, 735 

haemorrhage of, 735 

male, lesions of, 753 

malformations of, 735 

tumors of, 738 
Manneberg, resume of parasitic protozoa, 

ref, 127 
Marchand, giant cells, ref., 218 

hydatid moles, ref., 735 
Mast cells, 85 
Mastitis, 736 

Mays, myositis ossificans, ref., 782 
Measles, 274 
Mediastinum, 477 

inflammation of, 478 

tumors of, 478 
Megaloblasts, 79, 81 
Megalocytes, 81 
Melansemia, 86 
Megnin, parasites, ref., 142 
Melchior, cystitis, ref, 685 
Meltzer, empyema and subphrenic abscess, 

ref., 423 
Meningitis, 354 

acute cellular, 355 

acute exudative, 355 

cerebro-spinal, 199 

chronic, 358 

spinal, 390 

syphilitic, 362 

tuberculous, 359 
Merismopedia, 146 
Mesentery, cysts of, 588 

tumors of, 589 
Messmates, bacteria as, 152 
Metaplasia, 95 
Methyl-blue, Loffler's alkalin formula for, 

158 
Metritis, 707 

Meynert's method of opening brain, 15 
Microbes, safeguards of the body against, 

171 
Microcephalia, 388 
Micrococci, 144 
Microccoccus gonorrhoeas, 206 

tetragenus, 193, 261 
Microcytes, 79 



Micron, 144 
Micro-organ-isms, 143 

safeguards of the body against, 171 
Microscope, form of, for bacterial study, 158 
Microsporon furfur, 170 
Microtome, forms of, 60 
Miliary tubercles, 216 
Milk as culture medium, 161 
Miller, bacteria of mouth, ref., 538 
Mitosis, 93 

Moeller's method of spore staining, 155 
Moles, 735 

hydatid, 304 
Monte and Berggrun, anaemia of childhood, 

ref., 797 
Morbus maculosus, 798 
Mosselman and Liinaux, veterinary micro- 
biology, ref, 285 
Moulds, 143, 168, 170 
Mouth, bacteria in (footnote), 538 

gangrene, 535 

hypertrophy, 534 

inflammation, 534 

malformations, 533 

tumors, 535 
Mucous degeneration, 102 

membranes, pseudo-membranous in- 
flammation of, 204 

polyp, 303 
Mutter, leukaemia, ref., 796 

thyroid gland, structure of, ref, 639 
Miiller's fluid as hardening and preser- 
vative agent, 19, 53 
Muscle atrophy, 396, 783 

degeneration of, 783 

emboli, 780 

haemorrhage, 780 

hypertrophy, 787 

hypertrophy, pseudo-, 785 

inflammation, 780 

parasitic, 788 

regeneration, 780 

rupture, 780 

tumors, 787 

wounds, 780 
Museum specimens, preservation of, 63 
Mycelium in moulds, 168 
Mycosis, intestinal, 210, 577 

of pharynx, 284 
Myelitis, 397, 400 
Myelocytes, 85 
Myocarditis, 498 
Myocardium, fragmentation of, 493 

inflammation of, 498 
Myoma, 321 
Myomalacia, 493 



INDEX. 



839 



Myositis, chronic, 781 

ossificans, 781 

suppurative, 780 
Myxcedema, 641 
Myxoma, 300 

Naevi, vascular, 326 
Neck, cysts of, 538 
Necrosis, 96, 107 

coagulation, 96, 219 

fat, of pancreas, 634 

foci of, caused by bacteria, 172 

foci of, caused by toxins, 173 
.Neisser and Schaffer, gonococcus, ref., 208 
Nematoda, 135 

eggs of, 137 
Nephritis, acute diffuse, 655 

catarrhal, 650 

croupous, 650, 655 

desquamative, 650, 660 

diffuse, 655, 660 

-exudative, acute, 650 

glomerulo-, 650, 655 

indurative, chronic, 668 

interstitial, 668 

parenchymatous, 648, 650, 655, 659, 
660 

productive, 655, 660 

productive chronic, without exuda- 
tion, 668 

suppurative, 671 

tubal, 650 

tuberculous, 673 
Nerves, peripheral, inflammation of, 408 

peripheral, degeneration and regenera- 
tion, 408 

peripheral, tumors of, 409 
Nerve fibres, method of preservation of, 
22 

tissue, hardening and study of, 410 
Nervous system, 347 
Neuritis, 408 
Neuro-epithelioma, 340 
Neuroglia, character of, 294, 320 
Neuroma, 322 

false, 323 

multiple, 325 
Neuron, 393 

Nicolaier, capsulated bacillus, ref., 260 
Nikiforoff's method of fixing blood, 88 
Nissl's staining method, 412 
Nocard and Leclainche, animal infections, 

ref., 285 
Noma, 693, 697 
Normoblasts, 79, .81 
Northrup, tuberculosis in children, ref., 215 



Northrup, Crandall and, scorbutus in chil- 
dren, ref., 798 
Prudden and, etiology of pneumonia, 
ref., 449 
Novy, bacillus of malignant oedema, ref., 
259 
Vaughan and, ptomaines, ref., 174 
Noyes, sporadic cretinism, ref., 642 
Nucleus, changes in, during cell division, 

92 
Nuttall, Welch and, capsule bacillus, ref., 

261 
Nux vomica poisoning, 824 

Obermeier, spirochete of, 270 
Odontoma, 319 
(Edema, 71 

malignant bacillus of, 259 

of glottis, 416 

of lungs, 432 
(Esophagitis, 540 
CEsophagus, cysts of, 542 

dilatation, 541 

examination of, 29 

inflammation of, 540 

malformations, 538 

perforation, 541 

rupture of, 541 

stenosis of, 543 

tumors, 543 
Oestreich, fragmentation of heart muscle, 

ref., 493 
Oidium albicans, 170 
Oligocythsernia, 77, 78 
OUivier, lesions of typhoid, ref., 246 
Omentum, displacement of, 23 

lesions of, 578 
Oophoritis, 720 
Opium poisoning, 822 
Oppenheim, brain sclerosis, ref., 383 
Orchitis, 747 

Orth, spleen in leukaemia, ref., 771 
Osier, sporadic cretinism, ref., 642 
Osmic acid as hardening agent, 54, 56 
Osteitis, 757 

syphilitic, 762 

tuberculous, 761 
Osteoid tissue, 126 
Osteoma, 319 
Osteomalacia, 769 
Osteomyelitis, 763 
Osteophytes, 319 
Osteosclerosis, 760 
Ovaries, cysts of, 723 

displacements of, 719 

examination of, 40 



840 



INDEX. 




Ovaries, haemorrhage, 719 

hyperemia, 719 

inflammation of, 720 

malformations of, 719 

size of, 719 

tumors of, 722 
Oxyuris, 136 
Ozoena, bacteria in, ref., 538 

Pacchionian bodies, 11, 352 

Pachydermia laryngis, 414 

Pachymeningitis, 348 

Paget's disease, coccidia in, 129 

Paltauf, endothelioma of nerves, ref., 410 

Pancreas, concretions of, 635 

cysts of, 635 

degenerations of, 633 

displacements of, 636 

fat necrosis of, 634 

foreign bodies in, 635 

haemorrhage of, 632 

inflammation of, 632 

malformations of, 636 

situation, removal, examination, and 
preservation of, 37 

size and weight of, 37 

tumors of, 635 
Pancreatitis, 632 

Paoli, endothelioma of kidney, ref., 680 
Papilloma, 300 
Paraffin embedding, 58 
Parametritis, 707 
Paraphimosis, 743 
Parasites, 127 

animal, 127 

animal, methods of study, 142 

animal, bibliography, 142 

bacterial, 152 

vegetable, 143 
Parenchymatous degeneration, 98 
Paresis, general, of tissue, brain lesions, 385 
Park, diphtheria, etc., ref., 205 

chronic osteomyelitis, ref., 765 

fat embolism, 90 

and Beebe, diphtheria, ref., 252 

Biggs and Beebe, diphtheria, bacterio- 
logical diagnosis in, ref., 254 
Parotid gland lesions of, 637 
Parovarium, cysts of, 730 
Parsons, bone lesions of typhoid, ref., 246 
Pearls, epithelial, in carcinoma, 336 
Pediculus capitis, 141 
Penis, calcification, 744 

haemorrhage, 743 

inflammation, 743 

injury, 743 



Penis, malformation, 741 

tumors, 743 
Periarteritis nodosa, 507 
Pericarditis, 481 

tuberculous, 483 
Pericardium, air in, 480 

dropsy, 480 

haemorrhage, 480 

inflammation of, 481 

injuries, 480 

obliteration of, 482 

post-mortem examination of, 25 

tumors of, 483 
Perihepatitis, 611 
Perimetritis, 707 
Perinephritis, 676 
Periostitis, 755 
Perisplenitis, 628 
Peritoneum, 578 

inflammation, 579 

malformations of, 578 

parasites of, 589 

tumors, 587 
Peritonitis, acute, 579 

bacteria in, 582 

chronic, 583 

haemorrhagic, 585 

tuberculous, 586 
Petechiae, 70 

Petri's plates for bacteria cultures, 163 
Petruschky, bacteria in septicaemia, ref, 197 
Pfeiffer, Kitasato, and, Canon, influenza ba- 
cillus, ref., 257 
Phagocytes, 178 

in disposal of extra vasated blood, 71 

nature and action of, 126 
Pharyngitis, 540 
Pharyngo-mycosis, 284 
Pharynx, diverticula, 540 

inflammation of, 540 

malformations, 538 

removal from body, examination and 
preservation of, 29 

ulceration of, 541 
Phlebitis, 518 

tuberculous, 519 
Phleboliths, 73 

Phloroglucin for decalcification, 52 
Phosphorus poisoning, 817 
Phthisis, pulmonary, 459 

pulmonary, acute, 459 

pulmonary, chronic, 469 

pulmonary, experimental, 460 
Pia mater, 352 

haemorrhage, 354 

hyperaemia, 353 



INDEX. 



841 



Pia mater, inflammation, 354 

method of preservation of, 18 

oedema, 353 

parasites in, 364 

post-mortem examination of, 11 

spinalis, haemorrhage, 390 

spinalis, inflammation, 390 

spinalis, tumors and parasites, 391 

tumors, 362 
Picric acid for decalcification, 52 
Picro-acid fuchsin as staining agent, 61 
Pielicke, Canon and, bacillus of measles, 

ref., 271 
Pigmentation, 106 
Pineal gland, 369 
Pin worm, 136 
Pituitary body, 369 

degeneration, 734 

inflammation, 734 
Placenta, lesions of, 733 
Placentitis, 734 
Plague, bubonic, 239 
Plasmodium malarias, 129, 280 
Plate cultures of bacteria, 163 
Pleura, cysts of, 426 

haemorrhage of, 417 

hydrothorax, 417 

inflammation of, 417 

lymphangitis of, 423 

tumors of, 425 
Pleural cavities, method of post-mortem 
determination of presence of air in, 
24 

cavities, post-mortem examination of, 
28 
Pleurisy, 417 

chronic, 423 
Pleuritis, 417 

acute, 418 

chronic, 423 

tuberculous, 424 
Pneumococcus, 201, 438 

capsule, to stain, 203 
Pneumonatosis, 480 
Pneumonia, 438 

acute lobar, 201, 438 

broncho-, 442 

catarrhal, 443 

complicating, 448 

interstitial, 451 

interstitial, in phthisis, 472 

lobular, 443 

of heart disease, 449 

" organizing," 441 

secondary, 418 

syphilitic, 475 



Pneumonia, tuberculous, 452 
Pneumonitis, 438 
Pneumotoxin, 202 
Poikilocytes, 79 
Poisoning, autopsies in cases of, 41 

suspected, care of stomach and duode- 
num in, 35 
Poisons, action of, in body, 814 
Polaillon, lung stones, ref., 423 
Poliomyelitis anterior, 399 
Polyp, mucous, 303 
Popon, arsenic poisoning, 819 
Porencephalus, 380 
Portal vein, lesions of, 593 
Post-mortem bacterial examination, 167 

changes, 4 

changes in abdominal organs, 23 

cooling of the body, 6 

decomposition, 4 

discolorations, 4, 5, 23, 34 

examination in suspected poisoning, 
35, 41 

examination, internal, 9 

examination, medico-legal, 41 

examination, objects in, 3 

examination, observations on identity 
in, 4 

examination of abdomen, 30 

examination of brain, 11 

examination of new-born children, 
general inspection, 42 

examination of new-born children, in- 
ternal inspection, 46 

examination of spinal cord, 19 

examination of thorax, 22 

examination of wounds, 8 

examinations, external inspection, 4 

examinations, methods of making, 3 

examinations, weight of the body in, 5 

fractures, 9 

hypostasis, 5 

injuries, 8 

putrefaction, 5 

rigidity, or rigor mortis, 7 
Potash poisoning, 817 
Potassium nitrate poisoning, 817 
Potatoes, as culture media for bacteria, 162 
Pozzi, ovarian tumors, ref., 727 
Predisposition to infectious diseases, 176 
Pregnancy, extra-uterine, 732 
Preservation of tissues, importance of 
careful, 64 

of tissues, methods of, 52 
Productive inflammation, 117 
Progressive spinal muscle atrophy, 396 
Prostate, atrophy of, 752 



842 



INDEX. 



Prostate, concretion of, 753 

hypertrophy of, 751 

inflammation of, 752 

tumors of, 753 
Proteids, defensive, 178 
Protozoa, 127 
Prudden, cold on bacteria, 148 

endocarditis, malignant, ref., 495 

rhabdomyoma, ref., 638 
Psammoma, 312, 351, 363 
Pseudo-diphtheria, 204 
Pseudo-leukaemia, 796 
Pseudo-tubercles, 222 
Psorospermiae, 128 
Ptomaine poisoning, 825 
Ptomaines, 150 
Puerperal fever, 197 
Pulmonary phthisis, 459 
Purpura hemorrhagica, 798 
Pus cells, 117 

nature of, 116 
Putnam, nervous system in infectious dis- 
eases, ref., 377 
Putrefaction, post-mortem, 5 
Putrefactive changes in abdominal vis- 
cera, 23 
Pyaemia, 196 

Pyelitis, suppurative, 672 
Pyelo-nephritis, chronic, 672 

suppurative, 672 
Pye-Smith, cysts of liver, ref., 614 
Pyogenic bacteria, 188 
Pyo-pneumothorax, 422 
Pyo-salpinx, 731 

Rabies, 276 

Rabinowitsch, pathogenic yeasts, ref., 168 

thermophyllic bacteria, ref, 148 
Rachitis, 766 
Ray fungus, 263 
Rectocele vaginalis, 696 
Rectum, 573 

Reed, lymph nodules in typhoid, ref., 245 
Regeneration of tissues, 91 , 94 
Reinbach, colloid, ref., 640 
Relapsing fever, 269 
Respiratory system, 413 
Rhabdomyoma, 322 
Rhabdonema, 140 
Rheumatism, 803 
Rhexis, haemorrhage by, 69 
Rhinitis, membranous, ref., 538 
Rhinoscleroma, 238 
Rhizopods, 127 
Ribbert, appendicitis, ref., 575 

carcinoma, histogenesis, ref., 291 



Ribbert, lymph glands, ref., 526 

myoma, ref., 322 
Richer, yeasts and moulds, ref., 171 
Rickets, 766 
Rigor mortis, 7 
Robinson, cysts of mesentery, ref., 589^ 

Saccharomyces, 168 
Saccharomycetes, 143 
Salivary glands, 637 
Salpingitis, 731 
Salvetti, rachitis, ref., 767 
Saphrophytes, 152 
Sarcina, 146 
Sarcoma, 304 

adeno-, 312 

alveolar, 311 

angio-, 310 

chondro-, 312 

cysto-, 312 

endothelial, 312 

fibro-, 305 

giant-celled, 308 

glio-, 308 

lipo-, 312 

lympho-, 308 

melano-, 308 

mixed forms of, 311 

myeloid, 308 

•myo-, 312 

myxo-, 311 

osteo-, 309 

round -celled, 307 

spindle-celled, 305 
Sarcoptes, 141 
Savin poisoning, 821 
Scammony poisoning, 821 
Scarlatina, 273 
Scarlet fever, 273 

Scars, post-mortem, appearance of, 9 
Schamschin, heart lesions in diphtheria, 

ref., 250 
Schmidt and Aschoff, pyelonephritis, ref.„ 

685 
Schulz, endothelioma of pleura, 426 
Scirrhus, 341 
Scleroderma, 410 
Sclerosis, amyotrophic lateral, 396 

of spinal cord, 394, 400, 402 
Scolices of tapeworms, 131 
Scorbutus, 798 
Scrofula, 528 
Scrotum, lesions of, 744 
Section cutting, 56, 60 
Seminal vesicles, 751 
Septicaemia, 183, 196 



INDEX. 



843 



Septic intoxication, 174 
Serum, inflammatory, 112 

therapy in diphtheria, 253 
Seven-day fever, 269 
Shakespere, report on cholera, ref, 268 
Sherrington, bacteria in secretions, ref., 

178 
Ship fever, 275 

Silbermann, death from burning, ref, 807 
Silberschmidt, peritonitis, ref, 582 
Silver stain, Golgi's, 62 
Sittmann, bacterial study of blood, ref, 90 
Skull-cap, method of removal of, 10 
Small-pox, 271 
Soda poisoning, 817 
Spermatocele, 747 
Spider cells, 320 
Spina bifida, 407 
Spinal cord, bruising of, in removal, 20 

cysts of, 403 

degenerations of, 393 

dura mater of, lesions of, 387 

examination and preservation of, 19-21 

haeinatomyelia, 391 

hematomyelopore, 391 

haemorrhage, 391 

inflammation, 397 

injuries, 393 

malformations of, 405 

membranes of, 387 

parasites, 390 

pia mater, lesions of, 390 

progressive muscle atrophy of, 396 

sclerosis of, 326 

syringomyelia, 404 

tubercles of, 403 

tumors of, 39 r 
Spirillum, 144 

cholerse Asiaticse, 266 

fever, 269 
Spirochete Obermeieri, 270 
Spleen, accessory, 34 

anaemia of, 622 

atrophy of, 629 

bile duct, post-mortem examination 
of, 736 

congestion of, 623 

degenerations of, 629 

displacements of, 631 

examination and preservation of, 33 

hemorrhage of, 622 

hyperemia of, 622 

infarctions of, 623 

inflammations of, 624 

malformations of, 631 

parasites of, 630 



Spleen, pigmentation of, 630 

rupture of, 621 

sago, 629 

tumors of, 630 

wounds of, 621 
Splenic fever, 309 
Splenitis, 624 

Sporangium in moulds, 168 
Sporozoa, 128 
Spotted fever, 275 
Sprouting fungi, 143 
Sputum, tuberculous, number of bacilli in, 

223 
Staining, methods of, 60 
Staphylococcus epidermidis albus, 190 

cereus albus, 193 

cereus flavus, 193 

gilvus, 193 

pyogenes albus, 190 

pyogenes aureus, 188 

pyogenes citreus, 193 

salivarius pyogenes, 193 
Starr, multiple neuritis, ref., 409 
Stein, bladder tumors, ref, 686 

plates of cestoda, 142 
Stem, tumors in childhood, ref, 343 
Sternberg, discovery of pneumococcus by, 
201 

" Manual of Bacteria," ref, 182 

yellow fever studies, ref, 279 
Stoeltzner, cartilage in tonsils, ref., 543 
Stokes, Wright and, bacteriological exam- 
ination at autopsies, 168 
Stomach, appearance, post-mortem, of, 24 

care of, in cases of suspected poisoning, 
35 

degenerations of, 557 

dilatation of, 553 

erosions of, 553 

examination and preservation of, 35 

foreign bodies in, 557 

hemorrhage, 546 

inflammation, 547 

injuries, 546 

malformations, 546 

post-mortem changes, 546 

tumors of, 554 

ulcers of, 550-553 

wounds of, 546 
Stomacace, 534 

Stomatite ulcero-membraneuse, 534 
Stomatitis, 534 

Stoos, bacteria in angina, ref, 538 
Stramonium poisoning, 825 
Strangulation, 8, 810 
" Strawberry marks," 326 



844 



INDEX. 



Streptobacillus, 146 
Streptococcus, 195 

antitoxin, 193 

brevis, 191 

conglomerates, 191 

erysipelatis, 194 

in meningitis, 200 

longus, 191 

pyogenes/191, 204 
Stroebe, parasites in tumors, ref., 293 

regeneration in nerve tissue, ref., 377 
Strongylus, 136, 137 
Struma, 639 

lipomatosa suprarenalis, 645 
Strumitis, 640 
Strychnia poisoning, 824 
Sublimate, corrosive, as fixative agent, 

55 
Sublingual gland, lesions of, 637 
Submaxillary gland, lesions of, 637 
Sudcck, endothelioma of kidney, ref., 680 
Suffocation, 809 
Suggillations, 70 
Sunstroke, 806 
Suprarenal bodies, 32, 644 
Sutton, tumors, ref, 343 
Swab, sterilized, for bacteria collection, 166, 

167 
Symbiosis, 152 
Syphilis, 231 
Syringomyelia, 404 

Tabes, 402 
Taenia, 131-135 

echinococcus of liver, 614 
Tape-worms, 131 
Tartar emetic, poisoning by, 821 
Tattoo marks, post-mortem appearance 

of, 9 
Tavel, intestinal bacteria, ref, 573 

and Lanz, peritonitis, ref, 582 
Temperature, post-mortem, 6, 7 
Teratomata, 295 
Testicle, atrophy of, 745 

cysts of, 751 

inflammation of, 747 

malformations of, 745 

parasites of, 751 

tumors of, 750 

weight of, 38 
Tetano-toxin, 256 
Tetanus, 255 

Thacher, melanuria, ref, 308 
Thayer and Blume, bacteria in malignant 
endocarditis, ref, 495 

and Hewetson, malaria, ref, 283 



Thierf elder, endothelioma of pleura, ref., 

426 
Thiersch, carcinoma, ref, 291 
Thoma, nervous system malformations, 

ref, 388 
Thoma' s text-book, ref, 126 

microtome, 60 
Thompson, Addison's disease, ref, 801 
Thorax, examination of, 22, 25 
Thread worm, 136 

Thrombi, forms and occurrence of, 72 
Thrombosis, 72 

Thrombus, organization of, 124 
Thymus, 643 
Thyroid gland, examination of, 29 

exophthalmic goitre, 643 

lesions of, 639 

malformations of, 641 

myxcedema of, 641 

parasites of, 641 

regenerative power of, 95 
Tilger, cysts of pancreas, ref, 635 
Tissues, fresh, methods of study of, 50 

methods of preservation, 52 
Tongue, cysts of, 537 

hypertrophy of, 536 

inflammation of, 537 

malformations of, 536 

tumors of, 537 
Tonsillitis, 540 
Tonsils, faucial, 540 
Toxaemia, 174, 183 

ganglion cell changes in, 376 
Toxalbumins, bacterial, 151, 173 
Toxins, bacterial, 150, 173 
Trachea, malformations of, 413 

tumors of, 416 
Transudation, 71, 109, 112 
Trematoda, 130 

Triacid mixture of Ehrlich for blood stain- 
ing, 88 
Trichina spiralis, 138, 139 
Trichocephalus, 137 
Trichomonas vaginalis, 129 
Trichophyton tonsurans. 169 
Tubercle, 216 

bacilli, 213 

bacilli, action of, in lungs, 452 

bacilli, cultivation of, 214 

bacilli, dead, lesions caused by, 222 

bacilli, numbers of, in tuberculous 
sputum, 223 

bacilli, staining of, 224 

granulum, 217 

tissue, 217 
Tubercles, coagulation necrosis in, 219 



INDEX. 



S±z 



Tubercles, conglomerate, 217 

epithelioid-celled, 220 

forms of, 220 

lymphoid, 220 
Tuberculin, 221 
Tuberculosis, concurrent infection in, 224 

in the lower animals, 215 

localized, 215 
Tuberculous inflammation, 213. 216 
Tumors, archiblastic, 294 

cause of, 290 

classification of, 294 

congenital, 295 

cystic, 295 

epithelial, 358 

histioid, 291 

hypoblastic, 291 

inclusions of, 292 

malignancy, nature of, 289 

mesoblastic, 291 

metaplasia in, 317 

mixed, 295 

nature and growth of, 286, 287 

nomenclature of, 294, 297 

parablastic, 291 

parasitic origin of, 292 

preservation of, 298 

special forms of, 299 

spread of, 288 
Turpentine poisoning, 821 
Typhoid fever, 210 
Typhus fever, 275 

recurrens, 269 

11 rich, adrenals and adenoma of kidney, 

ref, 615 
Ureter, examination of, 30 
Ureteritis, 672 
Urethra, bacteria in, 690 

displacement of, 688 

inflammation of, 690 

malformations of, 688 

perforation, 689 

prolapse, 689 

rupture of, 689 

strictures of, 689 

tumors of, 691 

wounds of, 689 
Urethral hemorrhoids, 691 
Urethritis, 690 
Urinary apparatus, 676 

bladder, lesions of, 680 
Uterine hematocele, 703 
Uterus, cysts of, 718 

degeneration of, 709 

displacements of, 700 



Uterus, examination of, 39 
hyperemia of, 707 
hyperplasia of mucous membrane of, 

705 
inflammation, 701, 707, 708 
malformations of, 698 
parasites of, 718 
perforation of, 702 
rupture of, 702 
size, changes in, 699 
tumors of, 709 
ulceration of, 709 

Vagina, displacements of, 695 

gangrene of, 697 

hernia of, 695 

inflammation of, 697 

malformations of, 695 

parasites of, 698 

perforations of, 697 

prolapse of, 695 

tumors of, 697 

wounds of, 696 
Variola, 271 
Vascular system, 480 
Vaughan and Xovy, ptomaines, ref., 174 
Veins, dilatation of, 517 

inflammation of, 518 

parasites of, 520 

rupture of, 518 

tumors of, 520 

wounds of, 518 
Vein stones, 73 
Ventricles of brain, 365 
Veratria poisoning, 821 
Vermiform appendix, 573 
Vibrio of cholera, 266 
Virchow, tumors, ref., 313 
Van Gieson, false heterotopia, ref., 107 

hsematomyelopore, 392 

malformation of spinal cord, ref., 405 

picro-acid fuchsin, 61 

stain for amyloid hyalin, etc., 101 
Volkmann, endothelioma, ref, 316 
Von Hibler, gonococcus, ref., 208 
Von Kahlden, Addison's disease, 801 

endothelioma of kidney, ref., 680 

porencephalic ref., 380 
Von Limbeck, blood examination, 89 
Vulva, haemorrhage, 692 

hyperemia, 692 

inflammation, 693 

malformations, 692 

tumors, 691 

Wagner, endothelioma of pleura, ref.. 126 



846 



Waldeyer, cysts of ovaries, ref., 727 
Water, bacteria in, 151 

contamination of, with bacteria, 152 
Waxy degeneration, 100 
Weichselbaum, cysts of mesentery, ref., 589 

malignant endocarditis, ref., 495 
Weigert, adenoma of oesophagus, ref., 543 
modification of Gram's stain, 157 
stain for nerve tissue, 411 
Weihl, waxy degeneration of muscle, ex- 
perimental, ref., 787 
Weil's disease, 601 

Welch, Bacillus coli communis, ref., 260 
bacterial flora of body, ref., 171 
bacteriological examination at autop- 
sies, ref, 168 
infection and immunity, ref., 182 
modification of Guarnieri's agar for 

pneumococcus, 201 
oedema of lungs, ref., 433 
staining method for capsules of bac- 
teria, 203 
wound infection, ref., 190 
Welch and Flexner, Bacillus aerogenes cap- 
sulatus, ref., 261 
effects of diphtheria bacilli in animals, 
ref, 253 



/ 

INDEX. 

Whip worm, 137 

Wilks, kidney fibroma, ref., 677 

Williams, deciduoma, ref., 718 

ovarian papillomata, ref., 728 
Wilms, tumors of testicle, ref., 751 
" Wool-sorters' " disease, 309 
Wounds, 130 

healing of, 120 

post-mortem, 8 
Wright and Stokes, bacteriological examina- 
tion at autopsies, ref., 168 

Xylol, use of, in paraffin embedding, 58 



Yeasts, 143, 168, 170 
Yellow fever, 279 
Yersin, Calmette, and 
plague, ref., 239 



Borrel, bubonic 



Zaborowski, muscle regeneration, ref., 780 
Zahn, ciliated cysts, ref., 297, 543 

ciliated cysts of pleura, ref, 426 
Zenker, muscle degeneration, ref, 787 
Ziegler, views on catarrhal inflammation, 

114 
Zooglcea, 146 






▼ 



UBRARVOFCONGR^ 




007 635 457 1 • 



